* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Cooking Oils in Health and Disease - The Association of Physicians
Survey
Document related concepts
Waist–hip ratio wikipedia , lookup
Dietary fiber wikipedia , lookup
Epidemiology of metabolic syndrome wikipedia , lookup
Calorie restriction wikipedia , lookup
Low-carbohydrate diet wikipedia , lookup
Body fat percentage wikipedia , lookup
Fat acceptance movement wikipedia , lookup
Adipose tissue wikipedia , lookup
Abdominal obesity wikipedia , lookup
Diet-induced obesity model wikipedia , lookup
Transcript
Chapter 140 Cooking Oils in Health and Disease Shilpa Joshi, Shashank R Joshi INTRODUCTION World Health Report 2002 cites cardiovascular diseases (CVDs) as the largest cause of death and disability in India by 2020. This enormous burden is already evident in urban as well as semi-urban and slum dwellings across India, where increasing lifespan and rapid acquisition of adverse lifestyles related transition have contributed to rising prevalence of chronic disease determinants like smoking, physical inactivity, improper diet, stress, etc. and their ensuing outcomes such as obesity, hypertension and type 2 diabetes,thus having a significant impact on the national productivity. While fats are an essential part of a healthy balanced diet, there is an evidence to show that limiting saturated and trans fat intake is important, while it is prudent to have fat in your meals; it helps the body to absorb vitamins like vitamin A, D, E and K. It is a dense source of energy and of the essential fatty acids (EFAs) that the body cannot make. Too much saturated and trans fat contributes to the build-up of fatty material (plaque) inside the blood vessels (arteries). This process is called atherosclerosis and is a major cause of heart disease. Saturated fatty acid (SFA) and trans fats increase low-density lipoprotein (LDL) cholesterol in the blood, which leads to plaque formation. Polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) reduce LDL cholesterol and increase high-density lipoprotein (HDL) cholesterol. Saturated and trans fats in food causes a much greater increase in LDL cholesterol. MUFAs are beneficial in that they increase esterification of cholesterol in the liver, thereby reducing the free cholesterol pool and increasing receptormediated uptake of LDL cholesterol, resulting in a decrease in blood cholesterol levels as reported by the Dietary Guidelines Advisory Committee (DGAC) on the Dietary Guidelines for Americans, 2010. Evidence from controlled clinical studies has shown that MUFA favorably affect a number of risk factors for coronary heart diseases (CHDs), including plasma lipids and lipoproteins, factors related to thrombogenesis, in vitro LDL oxidative susceptibility and insulin sensitivity. Compared with SFA, MUFA lower total and LDL cholesterol levels, and relative to carbohydrate, they increase HDL cholesterol levels and decrease plasma triglyceride levels. Studies have shown that it is not a single fat source, but a combination of various fats having fatty acid compositions and additional minor components like tocotrienols, oryzanol and a good balance of SFA, MUFA and PUFA that will bring about favorable serum lipid profiles which help in guarding against suffering or mortality from CHD. Different oils have unique constituents like oryzanol, tocopherols, tocotrienols and phytosterols. Diverse effects of gamma-oryzanol have been reported, including the hypolipidemic effect. When 300 mg/day gamma-oryzanol was administered for 3 months to hyperlipidemic subjects, a significant decrease in plasma total cholesterol (TC) and LDL cholesterol was observed in both hypercholesterolemic and hypertrigly–ceridemic patients, while a relevant increase in HDL cholesterol was caused only in the hypercholesterolemic group. Thus, it is essential to choose the right quality of oils with diverse constituents which help to manage a healthier lifestyle. FAT BASICS Foods and nutrients provide the energy and building material for the countless substances that are essential to growth and survival of living things. The manner in which the nutrients become integral part of the body and contributes to its function depends on the physiologic and biochemical processes that govern their actions. Food invites consumption for a variety of reason; including form, texture, flavor as well as a host of physiological factors. Proteins, carbohydrates, fats all contribute to the total energy pool. Fat is an important component of diet and serve a number of functions in the body. Fat is a concentrated source of energy and it supplies per unit weight more than twice the energy furnished either by carbohydrate or protein. Dietary fats are stored in adipose tissue, which is a ready source of energy when food is unavailable. Functions of Fats • • • • • • • • They have high energy value Imparts palatability to diet Fats are precursors of biologically active compounds of the body Presence of fat is important for absorption of fat soluble vitamins like A, D, E Some fats called as EFAs have a vitamin-like function in the body They are constituents of body fluids and cell membranes Subcutaneous layer of fat insulates the body Fat pads at buttocks and palms protect the bones. OILS Introduction Although the words “oils”, “fats” are all used to refer to fats, “oils” is usually used to refer to fats that are liquids at normal room temperature, while “fats” is usually used to refer to fats that are solids at normal room temperature. The word “oil” is also used for any substance that does not mix with water and has a greasy feel. Types of Fats in Food Saturated fat is a fat that consists of triglycerides containing only SFAs. SFAs have no double bonds between the individual carbon atoms of the fatty acid chain. That is, the chain of carbon atoms is fully “saturated” with hydrogen atoms. Chapter 140 Cooking Oils in Health and Disease Section 19 Single bonds between carbon atoms are more stable than double bonds. Thus, compared to unsaturated fats, saturated fats are more stable and are usually solid at room temperature. The dietary sources of these fats include fat in milk, cream, butter, ghee, animal tallow and among vegetarian sources coconut oil, palm oil, etc. Many studies have found that consuming diets which are low in saturated fat reduces total and LDL cholesterol and also reduces the incidence of heart diseases. There is also a large evidence to show relation between higher SFA intake and prevalence of various kinds of cancer especially breast cancer and colorectal cancer. Also, there is enough evidence to prove that higher SFA intakes decreases insulin sensitivity. A higher intake of total and saturated fat is widely believed to contribute to the development of CHD. This belief is largely based on ecological studies relating dietary intake of saturated fat and rates of CHD. In the Seven Countries Study,1 intake of saturated fat as a percentage of calories was strongly correlated with coronary death rates across 16 defined populations in seven countries (r = 0.84). Interestingly, the correlation between the percentage of energy from total fat and CHD incidence was much weaker (r = 0.39). Indeed, the regions with the highest CHD rate (Finland) and the lowest rate (Crete) had the same amount of total fat intake, at about 40% of energy, which was the highest among the 16 populations. A followup data from Nurses’ Health study conducted a detailed prospective analyses of dietary fat and CHD among 80,082 women aged 34–59. This study showed that a 5% of energy from saturated fat, compared with equivalent energy from carbohydrates, was associated with a 17% greater risk of CHD [relative risk (RR) = 1.17, 95% confidence interval (CI) 0.97–1.41, p = 0.10]. It has been consistently shown in all studies that the possibility that the proportional increase in plasma HDL concentration produced by saturated fat somewhat compensates for its adverse effect on LDL level. In metabolic studies, different classes of SFAs have different effects on plasma lipid and lipoprotein levels2 specifically, SFAs with 12–16 carbon atoms tend to increase plasma total and LDL cholesterol levels, whereas stearic acid (18:0) does not have a cholesterol-raising effect in comparison with oleic acid (18:1). Among the cholesterol-raising SFAs, myristic acid (14:0) appears to be more potent than lauric acid (12:0) or palmitic acid (16:0),2 but the data are not entirely consistent.3 In a recent analysis of the Nurses’ Health Study,4 Hu and colleagues found that dietary intake of short to medium chain SFAs (4:0–10:0) was not significantly associated with risk of CHD [RR for a 1% increase in energy=0.97, 95% CI, 0.90–1.05]. In contrast, intakes of longer-chain SFAs (12:0– 18:0) were each separately associated with a small increase in risk (Table 1). In India, saturated fats are consumed as ghee (clarified butter) and coconut: as fresh, dry and as coconut oil along the coastal and southern parts of India. Milk products such as condensed milk (khoya), cream, full fat paneer are other sources of saturated fats. Cheese and also whole milk and its various products like milk shakes, ice creams, etc. form major source of saturated fats in urban India. PARTIALLY HYDROGENATED OR TRANS FATTY ACIDS These solid fats are made from mostly unsaturated vegetable oils (liquids) to which have been added some hydrogen atoms, through the process called hydrogenation, until the desired food characteristics of flavor, texture and stability are achieved. During the hydrogenation process, some hydrogen atoms change their configuration from being on the same side (cis) of a carboncarbon double bond to being on opposite sides (trans). If complete hydrogenation is achieved, there are no trans fats and saturated fats result. If only partial hydrogenation is obtained, some double bonds remain and transfats are produced. Trans fats were believed to have more structural stability and provide required texture to foods. Naturally occurring trans fatty acids (TFAs) are found in smaller amounts in beef and lamb. The positive relationship between trans fat intake and risk of CHD observed in the Nurses’ Health Study is generally consistent with several prospective studies conducted in men, including the Health Professionals’ Follow-up Study5 and the Alpha-Tocopherol Beta-Carotene Study. A higher intake of trans fat can contribute to increased risk of CHD through multiple mechanisms. First, TFAs raise LDL cholesterol levels6-9 and lower HDL cholesterol6-9 relative to cis unsaturated fatty acids. As such, the increase in the ratio of total to HDL cholesterol for trans fat is approximately double that for saturated fat.10 Second, trans fat increases lipoprotein (a) levels,11,12 which are positively associated with risk of CHD.13 Third, trans fat raises plasma triglyceride levels,14 and increased triglycerides are independently associated with increased risk of CHD.15,16 Fourth, TFAs can adversely affect EFA metabolism and prostaglandin balance by inhibiting the enzyme delta-6-desaturase and as a result, may promote thrombogenesis.17-19 Finally, recent data has suggested that high intake of trans fat may promote insulin resistance in humans.20 In India, trans fats are available as Vanaspati and Dalda. They are also present in stick margarines and shortening. Most of the food which is baked like cakes, cookies, pastries, puff, toast, khari, etc. have a large amount of TFA in them. Also, readymade mithais and ready to eat snacks like samosa, etc. tend to have a higher percentage of this fatty acid. Ready to eat and processed foods tend to have more trans fats in them. TABLE 1 │ Saturated fat profile of common foods; esterified fatty acids as percentage of total fat Food Lauric acid Myristic acid Palmitic acid Stearic acid Coconut oil 47% 18% 9% 3% Salmon 0% 1% 29% 3% Soybean oil 0% 0% 11% 4% Palm oil 0.1% 1% 44% 5% Cashews 2% 1% 10% 7% Eggs 0% 0.3% 27% 10% Butter 3% 11% 29% 13% Ground beef 0% 4% 26% 15% Dark chocolate 0% 1% 34% 43% Source: United States Department of Agriculture (2007) “USDA National Nutrient Database for Standard Reference, Release 20.” [online] Available from www.ars.usda.gov/ba/bhnrc/ndl. [Accessed December, 2012]. 639 Nutrition Section 19 UNSATURATED FATTY ACIDS An unsaturated fat is a fat or fatty acid in which there is at least one double bond is present within the fatty acid chain. A fat molecule is monounsaturated if it contains one double bond and polyunsaturated if it contains more than one double bond. Monounsaturated Fatty Acids These have fatty acids containing one double bond. As they have lesser double bonds as compared to PUFAs, they are less vulnerable to lipid peroxidation. Ecological studies have suggested an inverse association between monounsaturated fat intake and total mortality, as well as with CHD death.21 In particular, the mortality rate from CHD is very low in the traditional Mediterranean populations that use olive oil (a major source of oleic acid) as the primary source of fat.22 In metabolic studies, replacing carbohydrates with monounsaturated fat raises HDL without affecting LDL.23 This replacement may also improve glucose tolerance and insulin sensitivity among patients with diabetes mellitus.24 In addition, monounsaturated fat is resistant to oxidative modification.25 Dietary sources of MUFA are olive oil, groundnut oil, rice bran oil, mustard oil and canola oil. Lot of nuts like almonds, peanuts, etc. have high proportions MUFA in them. Fruits like olives and avocados are rich sources of MUFAs. These oils when used in prescribed amounts lower total cholesterol and LDL cholesterol levels in the blood. Polyunsaturated Fatty Acids Polyunsaturated lipids are triacylglycerols in which the hydrocarbon tails of this ester constitutes PUFA (fatty acids possessing more than a single carbon-carbon double bond). Numerous metabolic studies have shown strong cholesterol-lowering effects for vegetable oils rich in linoleic acid when substituted for dietary saturated fat.26 Also, dietary intervention trials using high-polyunsaturated fat diets have been more effective than those using low-fat high-carbohydrate diets in lowering total serum cholesterol as well as rates of CHD. Use of PUFA as fats is shown to reduce LDL cholesterol and improve insulin sensitivity. These are recommended fats for patients with cardiac diseases. Oils such as sunflower oil, safflower oil, corn oil are polyunsaturated fats. Besides these, all invisible fats present in cereals and pulses are also polyunsaturated. Although these fats lower cholesterol, they are not preferred to be used as visible fats. This is so because they are prone to oxidation in our body and secondly we consume them in large amounts as invisible fats in cereals and pulses. These PUFAs are of two types: 1. Omega-6 fatty acids (linoleic acid) 2. Omega-3 fatty acids. Omega-6 fatty acids (linoleic acid): This is a family of unsaturated fatty acids that have in common a final carbon-carbon double bond in the n-6 position, that is, the sixth bond, counting from the methyl end. As these fatty acids have greater number of double bonds they are prone to lipid peroxidation. In the Nurses’ Health Study, a higher intake of n-6 polyunsaturated fat was associated with a significantly lower incidence of type 2 diabetes.27 In addition, animal studies have suggested an anti arrhythmic effect when sunflower oil (rich in linoleic acid) was fed,28 although the effect was less than that when fish oil was fed. The Nurses’ Health Study also indicates that replacing long chain saturated fat with polyunsaturated fat is likely to substantially reduce the risk of CHD. In addition, when intakes of polyunsaturated and trans fat were considered together,28 the lowest risk of CHD was observed among those who were in the lowest quintile of trans fat and the highest quintile of polyunsaturated fat; the RR comparing women in this category with those with highest intake of trans fat and lowest intake of polyunsaturated fat was 0.31 (95% CI 0.11–0.88). These results indicate a substantial benefit to substituting polyunsaturated fat (such as unhydrogenated soybean or corn oil) for trans fat (such as hard margarine) in the diet or other foods high in TFAs. The dietary sources of these fatty acids are corn oil, kardi or safflower oil, sunflower oil, etc. Most of the cereal and pulses we consume have some amount of n-6/omega-6 fatty acid in them. These lower cholesterol and improve insulin sensitivity. Omega-6 fats are corn oil, kardi oil, sunflower oil and invisible fat in most of cereals and pulses. Omega-3 fatty acids: These are also called ω-3 fatty acids or n-3 fatty acids are fats commonly found in marine and plant oils. They are PUFAs with a double bond (C=C) starting after the third carbon atom from the end of the carbon chain. They are considered EFAs, meaning that they cannot be synthesized by the human body but are vital for normal metabolism. The plant sources of omega-3 fatty acids are green leafy vegetables (spinach, lettuce, broccoli, etc.), legumes (peas, split peas, pinto, etc.), citrus fruits and nuts (walnuts, hazelnuts, almonds). The animal sources of omega-3 fatty acids are fishes especially fatty fishes namely salmon, mackerel, anchovies, sardines and herring (Table 2). TABLE 2 │ The fat content of edible muscle tissue of fish consumed in India (g/100 g) Fatty fishes Fat (g/100 g) Fatty fishes Fat (g/100 g) Hilsa Purava Seer 19 6 4 Pomfret (white) Mackerel Bam Bombay duck Bhetki 1.3 1.8 0.9 0.8 0.8 MUFA PUFA (n-3) 25% 25% (mainly long chain) Lean fishes Pomfret (black) Murrel Katla Rohu 2.6 1.3 2.4 1.4 The approximate fatty acid composition of fish fats is: Saturates PUFA (n-6) 640 40% 10% Abbreviations: PUFA, Polyunsaturated fatty acid; MUFA, Monounsaturated fatty acid Chapter 140 Cooking Oils in Health and Disease Section 19 Most of the omega-3 fatty acid available from plant sources is in form of ALA (Tables 3 and 4). These get converted into long chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in human body through the desaturation-elongation chain pathway. Increased dietary consumption of ALA may decrease platelet aggregation and reduce formation of proaggregatory thromboxane A2 by inhibiting the conversion of linoleic acid (18:2, n-6) to arachidonic acid (20:4, n-6).30 Several epidemiologic studies have examined the association between ALA intake and risk of CHD. In the usual care group of the Multiple Risk Factor Intervention Trial,31 men in the highest quintile of ALA intake (expressed as percent of energy) had a 40% lower CHD mortality compared to men in the lowest quintile. In the Health Professionals Follow-up Study,5 a 1% increase in linolenic acid intake (expressed as percent of energy) was associated with a 40% lower risk of fatal CHD. In the Finnish Alpha-Tocopherol, BetaCarotene Cancer Prevention Study,32 men in the highest quintile of energy-adjusted ALA intake had 25% lower CHD mortality. In these three studies, however, the association between ALA intake and CHD was not the main focus, and none were adequately adjusted for other dietary factors, including intakes of other fats, dietary vitamins, folate and vegetables. In Nurses’Health Study, after adjusting for coronary risk factors, the RRs of fatal CHD from the lowest to highest quintiles of ALA intake. Given the strong evidence to support beneficial effects of ALA on CVD, flaxseed as well as other important dietary sources of ALA (e.g.unhydrogenated canola and soybean oils and walnuts) can be incorporated into a healthy and balanced diet for the prevention of CVD.33 A low rate of CVD in populations with very high intake of fish, such as Alaskan Native Americans,34,35 Greenland Eskimos36,37and Japanese living in fishing villages,38,39 suggests that fish oil may be protective against atherosclerosis. Subsequent prospective cohort studies have found an inverse association between fish consumption and risk of cardiovascular mortality in diverse populations. Krombout et al.40 demonstrated in the Dutch component of the Seven Countries Study, with 20 years of follow-up, those men who consumed 30 g of fish per day had a 50% lower CHD mortality than men who rarely ate fish. Two interventional studies, the Diet and Reinfarction Trial (DART)41 and the Gruppo Italiano per lo Studio della Sopravvivenza nell’ Infarto Miocardico (GISSI)-Prevenzione trial,42 have evaluated TABLE 3 │ The alpha-linolenic acid (ALA) content of various oils and foods Product Flaxseed oil Soy oil Canola oil Walnut, dry roasted Spinach Brussel sprouts Alpha-linolenic acid % by weight 50.8 7.0 9.3 6.8 0.12 0.20 TABLE 4 │ Rich sources of alpha-linolenic acid (ALA) Cereals and millets Pulses and legumes Vegetables Spices Oils Animal foods aLong Wheat, bajra Blackgram, cowpea (lobia), Rajmah, soya Green leafy Fenugreek (methi), mustard (rai) Mustard, soybean Fisha chain n-3 PUFA—biologically active product of ALA Source: Adapted from Diet and Heart Disease, National Institute of Nutrition. whether fish consumption or fish oil supplementation reduces coronary mortality among myocardial infarction (MI) patients. The DART, which included 2,033 men allocated to three dietary interventions, showed that subjects who received fish advice had a significant reduction in total mortality of 29% after 2 years. The GISSI-Prevenzione trial showed that supplementation with n-3 fatty acids resulted in a 10–15% reduction in the main endpoints (death, nonfatal MI and stroke). Most of the reduction was attributable to the decrease in cardiovascular death, especially sudden cardiac death. These two trials provide support for a therapeutic role of fish oil in the treatment of MI patients. The protective effects of marine n-3 fatty acids are probably due to multiple mechanisms, including reducing triglyceride levels,43 reducing platelet aggregation44 and antiarrhythmic effects.45 There is growing evidence to suggest that fish oil may improve endothelial dysfunction, an early marker of atherosclerosis.46,47 In vitro studies have consistently shown that n-3 fatty acids decrease expression of adhesion molecules on the endothelium and also decrease leukocyte/endothelium interactions.46 Additionally, clinical experi mental studies have shown that n-3 fatty acid supplementation improves endothelial-dependent vasomotor function.47,48 Ratio of Omega-6: Omega-3 Competition also exists among the families of PUFA for the elongase enzymes and for the acyltransferases involved in the formation of phospholipids. Because of the competitive nature of fatty acid desaturation and elongation, each class of EFA can interfere with the metabolism of each other. This competition has nutritional implications because these two classes of PUFA are metabolically and functionally distinct and have opposing physiological functions. Omega-3 (n-3) fatty acid is a structural component of membranes. Studies have shown that if n-3 fatty acid is unavailable, the body replaces it with another highly PUFA of the n-6 fatty acid series. This maintains the overall polyunsaturated content of the membrane, but the structure is not at its optimum. n-6 fatty acid series cannot be converted into n-3 fatty acid in the human body and thus they cannot perform the functions that n-3 fatty acids. n-3 and n-6 fatty acids are precursors of eicosanoids, which regulate many of body function. Eicosanoids derived from n-3 fatty acid are homologous to of those derived from n-6 fatty acid with which they compete and they are associated with less proinflammatory response than n-6 eicosanoids which bound to specific receptors. Balance between n-6 fatty acid and n-3 fatty acid series is required for proper functioning of body. The current high intake of n-6 PUFA may be undesirable because of ensuing high concentration of arachidonic acids may be conducive to enhanced or imbalanced eicosanoids production in sensitive cells even in response to normal physiological stimuli. This may result in high responsiveness, if chronic; it may gradually initiate or exacerbate several pathophysiological conditions. In short, an extreme diet in which almost the entire dietary fat comes from n-6 PUFA such as corn oil seems to be undesirable. Lopsided diet consumed during the last few decades altered the ratio to as much as 25 to 1. The body adjusted apparently well to such liberties, but gradually the possible ill effects of the drastic change are being realized. Therefore, it is now proposed to restore the n-6 to n-3 ratio to at least 10 to 1. CHOLESTEROL Cholesterol is waxy sterol of fat. Cholesterol is essential for animal life; animal fats have cholesterol in them. Animal fats like butter, cream, ghee and nonvegetarian foods like egg, meats, etc. have cholesterol in them. Organ meats like liver and brain are rich sources of dietary cholesterol. Plants usually make cholesterol in very small amounts 641 Nutrition Section 19 TABLE 5 │ Fatty acid composition and cholesterol content of animal foods* (g/100 edible portion) Item Fat g/100 g Saturated fatty acids g/100 g Cholesterol mg/100 g Butter Ghee Milk (cow) Milk (buffalo) Milk (skimmed) Milk (condensed) Cream Cheese Egg (whole)a Egg yolk Chicken without skin Chicken with skin Beef Mutton Pork 80 100 4 8 0.1 10 13 25 11 30 4 18 16 13 35 50 65 2 4 6 8 15 4 9 1 6 8 7 13 250 300 14 16 2 40 40 100 400 1,120 60 100 70 65 90 Organ meats: Brain Heart Kidney Liver 6 5 2 9 2 2 1 3 2,000 150 370 300 2 1.5 6 0.3 0.4 2.5 150 45 45 Fresh water and sea foods: Prawns/Shrimps Fish (lean) Fish (fatty) *Value vary depending on the feed of the animals aOne whole egg or yolk of one egg contains 210 mg cholesterol. Source: Gopalan, et al. 1989; McCance and Widdowson, 1993 and hence plant-basedoils do not have cholesterol in them. Plants manufacture phytosterols, which can compete with cholesterol for absorption in the intestine, thus probably reducing the absorption of dietary cholesterol. It is advisable to limit intake of dietary cholesterol to 200 mg or less. This can be achieved by limiting animal-based fat and limiting consumption of nonvegetarian foods. Dietary cholesterol raises LDL cholesterol levels and very high intakes cause atherosclerosis in numerous animal models.49 In controlled metabolic studies conducted in humans, dietary cholesterol raises levels of total and LDL cholesterol in blood,50,51 but the effects are relatively small compared with saturated and TFAs,52,53 and individuals vary widely in their responses.54 A significant positive association between dietary cholesterol and CHD was found in some epidemiologic studies, but not in others (Table 5).5 CHOOSING THE RIGHT OIL Selection of cooking medium depends on three factors. The fatty acid profile of the oil, the micronutrients which come along with it. As per recommendation the preferred cooking medium is a monounsaturated fat. As about 15% of visible fat should come from MUFA. Therefore, recommended cooking oils would be groundnut oil, rice bran oil, canola oil, mustard oil, etc. None of the above cooking medium gives a desirable fatty acid profile as most the fats which contain MUFA do not contain appropriate ratios of omega-3 fatty acids. For this reason, it is better to rotate oils while using and also use nuts which contains these fatty acids. By limiting the visible fat content of diet and including oilseeds in the diet the fatty acid profile of the whole diet can be changed (Table 6). 642 QUANTITY OF OIL Quantity of oil used is as important as the quality of fat. It is important to limit the quantity of fats however good the quality of fat is. This is so because fats are high in calories and every gram increase in fat intake results in caloric overload. Also, high-fat diet increases the total cholesterol and decreases insulin sensitivity. The recommendation by Indian Council of Medical Research (ICMR) is that about 25–30% calories should come from fat. There is a lot of invisible fat consumed in Indian diet. This leaves about 25–30 g of fat per day in form of visible oils. It is recommended that among this fat allowance some portion of fat should be consumed in form of nuts which are rich in omega-3 fatty acids like walnuts and flaxseeds. Remaining 15–20 g per day or 3–4 teaspoons should be used as cooking fat/edible fat. OIL USAGE Oil should not be over heated or smoked to prevent it from rancidity and oxidation. Also over heating or frying of oils causes formation of oxidation products like peroxides, hydroperoxides and secondary products like aldehydes and other volatile compounds which have implication in heart diseases, cancers, etc. Hence, it is important not to reuse the fried oil and also using cooking met hods which do not encourage heating of oils to high temperature. PUFA are especially prone to oxidation faster and at a much lower temperature than other oils. VISIBLE AND INVISIBLE FATS Most important part of controlling fat intake is recognizing fat containing foods. There are lots of foods which contain a very high proportion on invisible fats. Desirable invisible fats are present in Chapter 140 Cooking Oils in Health and Disease Section 19 TABLE 6 │ Approximate fatty acid composition of common fats and oils (g/100 g) Coconut* Palm kernel Gheea,b Vanaspatib Red palm oil (raw) Palm oil Olive Groundnut Rape/Mustardc Sesame Rice bran Cotton seed Corn Sunflower Safflower Saturated Monounsaturated Linoleic Alpha-linolenic Predominant fatty acids 90 82 65 24 50 45 13 24 8 15 22 22 12 13 13 7 15 32 19 40 44 76 50 70 42 41 25 32 27 17 2 2 2 3 9 10 10 25 12 42 35 52 55 60 70 <0.5 <0.5 <1.0 <0.5 <0.5 <0.5 <0.5 <0.5 10 1.0 1.5 1.0 1.0 <0.5 <0.5 Saturated Saturated Saturated Saturated Saturated + Monounsaturated Saturated + Monounsaturated Monounsaturated Monounsaturated Monounsaturated Mono and polyunsaturated Mono and polyunsaturated Polyunsaturated Polyunsaturated Polyunsaturated Polyunsaturated aMainly, short and medium chain fatty acids* (Coconut 77%, ghee 25%) fatty acids (Ghee 2%, vanaspati 53%) cLong chain MUFAs (50% eruric acid and 5% eicosenoic acid) Source: Adapted from Diet and Heart Disease, National Institute of Nutrition. bTrans TABLE 7 │ Recommendation for fatty acids and calories Total fat <30 % of total calories Step I diet Step II diet Up to 10% of total calories 8–10% of total calories Up to 10% of total calories <7% of total calories Up to 10% of total calories Up to 15% of total calories Up to 15% of total calories Up to 15% of total calories Carbohydrates 55% or more of total calories 55% or more of total 55% or more of total Protein Approximately 15% of total calories Approximately 15% of total calorie Approximately 15% of total calorie <300 mg/day <200 mg/day To achieve and maintain desirable weight To achieve and maintain desirable weight Saturated fatty acids Polyunsaturated fatty acids Monounsaturated fatty acids Cholesterol Total calories* To achieve and maintain desirable weight *Calories from alcohol not included. Source: Data from National Cholesterol Education Program (NCEP). Second Report of the Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). NIH Publication No.93-3095, Bethesda, MD: National Institutes of Health. National Heart, Lung and Blood Institute; 1993. nuts and oilseeds. While it is recommended that diet should contain oils and seeds, it important to reduce the visible fat content of the diet when these are included. Many types of foods like precooked, processed foods, ready to eat snacks contain lot of fats in them. This is especially true of bakery products like biscuits, cookies, Khari, puff pastries which form an important part of diet of Indians with their morning and evening tea. Other very rich source of invisible fats is papads, pickles, chutney and other condiments which are used liberally in Indian diets. These should be considered before recommending quantity of fat. Recommendation for Fats (Table 7) American Heart Association and National Cholesterol Education Program recommend that the fat which should be predominant in our diets should be monounsaturated. WHY BLENDS ARE NEEDED? Dietary fat plays an important role in cardiovascular health. Numerous studies have been carried out to identify the type of fat that correlates with the CVD. Excessive intake of saturated fat raises total and LDL cholesterol levels.1 It also has a negative effect on blood pressure and arrhythmias.2 TFAs generated during partial hydrogenation of fat can elevate LDL cholesterol and reduce HDL cholesterol.3 Whereas monounsaturated fat is neutral when substituted with carbohydrates. The greatest CVD risk reduction is associated with PUFA intake whereas a lesser risk reduction is associated with monounsaturated fat.1 However, substitution of MUFA to PUFA results in formation of LDL which are less susceptible to oxidation.4 Both n-6 (linoleic acid) and n-3 (ALA) PUFAs are protective. Linoleic acid has profound effect on lowering LDL cholesterol.1 Long chain omega-3 fatty acids are hypotriglyceridemic. There are various mechanisms through which long-chain omega-3 fatty acids exerts positive effect on heart health like antiarrhythmic effect, decreased platelet aggregation, vasodilatation, anti-inflammatory effects, etc. It also improves endothelial function and reduces collagen deposition.5 Hence, optimum balance of these fat components is necessary to achieve favorable effect on health. 643 Nutrition Various institutions, health governing bodies have given various recommendations for fatty acid intake. National Institute of Nutrition, Hyderabad, suggests that “Fat from varied source is better than any single kind.” Guidelines to prevent heart disease have given upper limits for SFAs are 8–10% of total calories, PUFAs should be 5–8% of total calories and MUFA would contribute the difference. The desirable PUFA: SFA ratio is about 0.8–1 and PUFA includes both the types (omega-6 and omega-3) as to provide linolenic acid (LA) to ALA ratio of 5–10.2 Joint Food and Agriculture Organization/World Health Organi zation (FAO/WHO) Expert Consultation (2008) suggests that minimum total fat intake should be 15% of total energy for men and 20% of total energy for women and maximum total intake is 30–35% energy. It is recommended that total intake of SFAs should not exceed 10% of energy. The range given for PUFA intake is 6–11% of energy. MUFA will contribute the difference, i.e.total fat intake (%E) – SFA (%E) – PUFA (%E) – TFA (%E). Hence, if maximum total fat intake is taken into consideration, ratio of SFA: MUFA: PUFA get derived to 1:1.5:1.6 Diet and lifestyle recommendations from American Heart Association (AHA) (2006) provide guidance to reduce risk for CVD. AHA recommends intakes of less than7% of energy as saturated fat, less than 1% of energy as trans fat and less than 300 mg cholesterol per day. Oils and fats (visible fat) plays an important role in total dietary fat intake.7 Unfortunately, there is no single oil available which can satisfy suggested guidelines. Blending two oils also cannot give you required ratio. Hence, there a need to develop blends using more than two oils to provide health benefits. REFERENCES 1. Keys AB. Seven countries: a multivariate analysis of death and coronary heart disease. Cambridge, MA: Harvard University Press; 1980. 2. Kris-Etherton PM, Yu S. Individual fatty acids on plasma lipids and lipoproteins: human studies. Am J Clin Nutr. 1997;65 (5 Suppl):1628S-44S. 3. Temme EH, Mensink RP, Hornstra G. Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men. Am J Clin Nutr. 1996;63(6):897903. 4. Hu FB, Stampfer MJ, Manson JE, et al. Dietary saturated fat and their food sources in relation to the risk of coronary heart disease in women. Am J Clin Nutr. 1999;70(6):1001-8. 5. Ascherio A, Rimm EB, Giovannucci EL, et al. Dietary fat and risk of coronary heart disease in men: cohort follow-up study in the United States. BMJ. 1996;313(7049):84-90. 6. Judd JT, Clevidence BA, Muesing RA, et al. Dietary trans fatty acids: effects of plasma lipids and lipoproteins of healthy men and women. Am J Clin Nutr. 1994;59(4):861-8. 7.Lichtenstein AH, Ausman LM, Carrasco W, et al. Hydrogenation impairs the hypolipidemic effect of corn oil in humans. Aterioscler Thromb. 1993;13(2):154-61. 8. Mensink RP, Katan MB. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med.1990;323(7):439-45. 9.Zock PL, Katan MB. Hydrogenation alternatives: effects of trans fatty acids and stearic acid versus linoleic acid on serum lipids and lipoproteins in humans. J Lipid Res. 1992;33(3):399-410. 10. Willett WC, Ascherio A. Trans fatty acids: are the effects only marginal? Am J Public Health. 1994;84(5):722-4. 11. Nestel P, Noakes M, Belling Bea. Plasma lipoprotein and Lp[a] changes with substitution of elaidic acid for oleic acid in the diet. J Lipid Res. 1992;33(7):1029-36. 12. Sundram K, Ismail A, Hayes KC, et al. Trans (elaidic) fatty acids adversely affect the lipoprotein profile relative to specific saturated fatty acids in humans. J Nutr. 1997;127(3):514S-20S. 644 Section 19 13. Utermann G. The mysteries of lipoprotein (a). Science. 1989; 246(4932):904-10. 14. Katan MB, Zock PL, Mensink RP. Trans fatty acids and their effects on lipoproteins in humans. Annu Rev Nutr.1995;15:473-93. 15. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3(2):213-9. 16. Stampfer MJ, Krauss RM, Ma J, et al. A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. JAMA. 1996;276(11): 882-8. 17. Hill EG, Johnson SB, Lawson LD, et al. Perturbation of the metabolism of essential fatty acids by dietary partially hydrogenated vegetable oil. Proc Natl Acad Sci USA. 1982;79(4): 953-7. 18. Kinsella JE, Bruckner G, Mai J, et al. Metabolism of trans fatty acids with emphasis on the effects of trans, trans-octadecadienoate on lipid composition, essential fatty acid, and prostaglandins: an overview. Am J Clin Nutr. 1981;34(10): 2307-18. 19. Jones D. Trans fatty acids and dieting. Lancet. 1993;341(8852): 1093. 20. Lovejoy JC. Dietary fatty acids and insulin resistance. Curr Atheroscler Rep. 1999;1(3): 215-20. 21. Jacobs D, Blackburn G, Higgins M, et al. Report of the Conference on Low Blood Cholesterol: Mortality Associations. Circulation. 1992;86(3):1046-60. 22. Grundy SM, Bilheimer D, Blackburn H, et al. Rationale of the dietheart statement of the American Heart Association. Report of Nutrition Committee. Circulation. 1982;65(4):839A-54A. 23. Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb. 1992;12(8):911-9. 24. Garg A, Grundy SM, Koffler M. Effect of high carbohydrate intake on hyperglycemia, islet cell function, and plasma lipoproteins in NIDDM. Diabetes Care.1992;15(11):1572-80. 25. Parthasarathy S, Khoo JC, Miller E, et al. Low density lipoprotein rich in oleic acid is protected against oxidative modification: implications for dietary prevention of atherosclerosis. Proc Natl Acad Sci USA. 1990;87(10):3894-8. 26. Hu F, Salmeron J, Manson J, et al. Dietary fat and risk of type 2 diabetes in women. Am J Epidemiol. 1999;149:S1. 27. Abeywardena MY, McLennan PL, Charnock JS. Differential effects of dietary fish oil on myocardial prostaglandin I2 and thromboxane A2 production. Am J Physiol. 1991;260(2 Pt 2): H379-85. 28. Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and risk of coronary heart disease in women. N Engl J Med. 1997;337(21):1491-9. 29. Adam O, Wolfram G, Zöllner N. Effect of alpha-linolenic acid in the human diet on linoleic acid metabolism and prostaglandin biosythesis. J Lipid Res. 1986;27(4):421-6. 30. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med. 1992;200(2):177-82. 31. Pietinen P, Ascherio A, Korhonen P, et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol.1997;145(10): 876-87. 32. Connor WE. Alpha-linolenic acid in health and disease. Am J ClinNutr. 1999;69(5):827-8. 33. Newman WP, Middaugh JP, Propst MT, et al. Atherosclerosis in Alaska natives and non-natives. Lancet. 1993;341(8852):1056-7. 34. Middaugh J. Cardiovascular deaths among Alaskan Natives, 1980-86. Am J Public Health. 1990;80(3):282-5. 35. Kromann N, Green A. Epidemiological studies in Upernavik district, Greenland. Incidence of some chronic diseases 1950-1974. Acta Med Scand. 1980;208(5):401-6. 36. Bang HO, Dyerberg J, Hjøorne N. The composition of food consumed by Greenland Eskimos. Acta Med Scand. 1976;200(1-2):69-73. 37. Hirai A, Hamazaki T, Terano T, et al. Eicosapentaenoic acid and platelet function in Japanese. Lancet. 1980;2(8204):1132-3. 38. Kagawa Y, Nishizawa M, Suzuki M, et al. Eicosapolyenoic acids of serum lipids of Japanese islanders with low incidence of cardiovascular disease. J Nutr Sci Vitaminol (Tokyo). 1982; 28(4):441-53. 39. Kromhout D, Bosschieter EB, de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med. 1985; 312(19):1205-9. Section 19 40. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. 1989;2(8666):757-61. 41. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infartomio cardico: Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results from the GISSIPrevenzione trial. Lancet. 1999;354(9177):447-55. 42. Harris WS. Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review. J Lipid Res. 1989;30(6): 785-807. 43. von Shacky C. n-3 fatty acids and the prevention of coronary atherosclerosis. Am J Clin Nutr. 2000;71(1 Suppl):224S-7S. 44.Kang JX, Leaf A. Prevention of fatal cardiac arrhythmias by polyunsaturated fatty acids. Am J Clin Nutr. 2000;71(1 Suppl): 202S-7S. 45. DeCaterina R, Liao JK, Libby P. Fatty acid modulation of endothelial activation. Am J Clin Nutr. 2000;71(1 Suppl):213S-23S. 46. Goodfellow J, Bellamy MF, Ramsey MW, et al. Dietary supplementation with marine omega-3 fatty acids improve systemic large artery endothelial function in subjects with hypercholesterolemia. J Am Coll Cardiol. 2000;35(2):265-70. 47. Fleischhauer FJ, Yan WD, Fischell TA. Fish oil improves endotheliumdependent coronary vasodilation in heart transplant recipients. J Am Coll Cardiol. 1993;21(4):982-9. Chapter 140 Cooking Oils in Health and Disease 48. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease. Arch Pathol Lab Med. 1988;112(10):1032-40. 49. Keys A, Parlin RW. Serum cholesterol response to changes in dietary lipids. Am J Clin Nutr. 1966;19(3):175-81. 50. Hegsted DM, McGandy RB, Myers ML, et al. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr. 1965;17(5):28195. 51. Clarke R, Frost C, Collins R, et al. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997;314(7074):112-7. 52.Howell WH, McNamara DJ, Tosca MA, et al. Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. Am J Clin Nutr. 1997;65(6):1747-64. 53. McGill HC. The relationship of dietary cholesterol to serum cholestrol concentration and to atherosclerosis in man. Am J Clin Nutr. 1979;32(12 Suppl):2664-702. 54. Kris-Etherton P, Daniels SR, Eckel RH, et al. Summary of the scientific conference on dietary fatty acids and cardiovascular health: conference summary from the nutrition committee of the American Heart Association. Circulation. 2001;103(7):1034-9. 645