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 Palm Oil Is A Popular And Beneficial Cooking Ingredient
Palm oil is produced from the fruit of the Elaeis guineensis tree. It is a vegetable oil, not an animal or dairy product, and therefore does not contain cholesterol. Palm oil sometimes is confused with palm kernel oil, but in fact is quite different, being made from the mesocarp of the palm fruit rather than the hard center kernel. Palm oil contains much less saturated fat than palm kernel or coconut oil. Palm oil has been used in food preparation for over 5,000 years. Today it is consumed worldwide as a cooking oil, margarine and shortening, and also is used as an ingredient in fat blends and a vast array of food products. In the United States, palm oil's principal edible use is as an ingredient in prepared foods (primarily baked goods). Food manufacturers choose palm oil because it has a distinctive quality, requires little or no hydrogenation, and lengthens the shelf life of products. These advantages are difficult to duplicate at the same cost with polyunsaturated oils, which often have higher market prices and require additional processing such as hydrogenation for the same characteristics. The Unjustified “Health Scare” Over Palm Oil Despite the prominent position of palm oil in world markets, it was not marketed extensively in the United States until the early 1980s. By 1985, palm oil had garnered a two percent share of the American market, which is dominated by soybean oil (with over 70% of the market). Palm oil became the target of a massive negative advertising campaign, including widely-published allegations that palm oil is “hazardous to your health.” Advertisements likened palm oil to a lit bomb that could “kill” Americans. Palm oil also was the victim of letter-writing campaigns to food companies complaining of palm oil's allegedly adverse health effects. Legislation was introduced in 1987 to discriminate against tropical oils by imposing special labeling restrictions on food products containing them. The bill was withdrawn following stiff opposition, including criticism by the FDA, the United States Trade Representative, and the scientific community. The campaign against palm oil was unprecedented. Even though palm oil is widely used throughout the world, no governmental body ever labeled it as unhealthful. FDA criticized the negative advertising campaign. For example, Dr. Edward Scarbrough, who until recently headed FDA's Center for Food and Nutrition Safety, cautioned that “[s]ingling out [tropical oils] . . .is unlikely to lead to any meaningful reduction in the incidence of coronary disease.”[i] Beginning in 1991, FDA began taking enforcement action against food manufacturers making “no palm oil” and “no tropical oils” label claims. FDA issued warning letters to The Kroger Company[ii] and Goodmark Foods, Inc.,[iii] notifying the companies that “no palm oil” and “no tropical oils” label claims on baked goods containing saturated or hydrogenated fats and oils were false and misleading, and violated § 403(a)(1) of the Federal Food, Drug and Cosmetic Act. Following passage of the Nutrition Labeling and Education Act of 1994, FDA issued regulations prohibiting claims such as “no palm oil” and “no tropical oils” from food labels, unless and until pre-approved by FDA through a petition process. See 21 C.F.R. § 101.69. FDA has not pre-approved “no palm oil” or “no tropical oils” claims. Manufacturers that display these claims on food labels are in violation of § 403(a)(1), and subject to disciplinary action by FDA and penalties. Palm Oil Does Not Raise Health Concerns Typically Associated With Saturated Fats Palm oil has been attacked as being “saturated,” because it contains 44% palmitic acid and 5% stearic acid, and thereby allegedly raises blood cholesterol and increases the risk of cardiovascular disease. A sizable and growing body of scientific evidence, indicates, however, that palm oil's effect on blood cholesterol is relatively neutral when compared to other fats and oils. In a survey article, Professor Charles Elson concluded, “palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet.”[iv] Many pre-1990 human feeding studies reported that palm oil diets resulted in lower serum cholesterol levels than pre-study values.[v] Five distinguished American scientists concluded that these studies “have revealed that a palm oil diet lowered plasma cholesterol compared with the starting periods during which the subjects were eating their habitual Western diets.”[vi] Subsequent studies, specifically designed to evaluate palm oil, confirm that palm oil's impact on serum lipid and lipoprotein profiles compares favorably to corn oil, hydrogenated soybean oil, and olive oil.[vii] A 1995 study comparing the effect of palm olein and olive oil diets on twenty-one healthy, free-living normocholesterolemic subjects found no difference in total and LDL-cholesterol levels.[viii] In sum, the scientific evidence reveals that palm oil affects serum lipids more like a monounsaturated than a saturated oil. There appear to be a number of explanations. Palm oil contains a high percentage of monounsaturates (40%). Its saturated fatty acids are palmitic (90%), which does not appear to elevate blood cholesterol in people with cholesterol levels in normal ranges,[ix] and stearic (10%), which also does not raise blood cholesterol concentrations.[x] Animal studies have found that palm oil stimulates synthesis of protective HDL cholesterol and removal of harmful LDL cholesterol.[xi] In addition, palm oil is rich in vitamin E and particularly in tocotrienols, whose health benefits appear to include the reduction of serum cholesterol concentrations.[xii] It also appears that palm oil, as compared to saturated fats and oils, may pose a lesser degree of risk of cancer,[xiii] or thrombosis.[xiv] This may be due to tocotrienols[xv] or other phytonutrients[xvi] present in palm oil. Indeed, Professors K. K. Carroll of the Centre for Human Nutrition at the University of Western Ontario and David Kritchevsky of the Wistar Institute recently concluded that evidence from animal and in vitro studies indicate that tocotrienols of palm oil are effective anti-cancer agents and provide adequate justification for clinical trials in human cancer patients. Palm oil is the only vegetable oil available on the world market that naturally contains tocotrienols. Substitution Of Hydrogenated Oils And Fats For Palm Oil Does Not Produce A More Healthful Product Palm oil's desirable texture and stability stem primarily from its saturatedness. Substitute products must be processed by blending or hydrogenation to achieve a comparable degree of saturatedness. Hydrogenation transforms unsaturated fatty acids into saturates and creates more than a dozen unnatural fatty acids.[xvii] As noted above, FDA has issued warning letters to food manufacturers that a “no tropical oils’’ claim is false and misleading for a product that contains hydrogenated fats and oils. FDA officials also have lamented in testimony before Congress that consumers are left no better off when processed oils are substituted for tropical oils:[xviii] It is very likely that if we replace one of the tropical oils in [a] particular product, . . .the oil technologist will change whatever oil he replaces that with to have generally these same characteristics, so that if saturation is a problem, it will probably remain a problem in that product. Dr. Scarbrough, who until recently headed FDA's Center for Food and Nutrition Safety, stated “campaigns [against tropical oils] ignore the effects of hydrogenation and blending of the fatty acid content of most oils used in processed foods.”[xix] In November 1999, after years of study and deliberation, FDA issued proposed regulations requiring disclosure of trans fat on food labels, and limiting the types of claims regarding trans fat that are allowed on food labels.[xx] In a comprehensive review of available scientific evidence, FDA concluded that trans fats increase the risk of cardiovascular disease, and that Americans’ dietary intake of trans fats is high enough to warrant “serious attention from a public health perspective.”[xxi] In July 2003, FDA issued final regulations requiring food manufacturers to disclose trans fat content on the Nutrition Facts label beginning January 1, 2006, and limiting labeling claims that can be made about foods which are high in trans fat.[xxii] FDA’s regulatory action represents the culmination of years of concern about trans fatty acids in the scientific and public health communities.[xxiii] Today there is abundant scientific evidence that trans fatty acids negatively affect serum lipid profiles. Professor Scott Grundy concluded that there is “convincing evidence that trans monounsaturated fatty acids definitely raise LDL cholesterol levels, in a manner similar to that of the cholesterol-raising saturated fatty acids.”[xxiv] A Dutch human study concluded, “[t]he effect of trans fatty acids on the serum lipoprotein profile is at least as unfavorable as that of the cholesterol-raising saturated fatty acids, because they not only raise LDL cholesterol levels but also lower HDL cholesterol levels.”[xxv] More recently, Professor Grundy observed:[xxvi] It has been estimated that the average intake of transmonounsaturates in the American diet is six to eight grams a day. * * * [T]his intake * * * will produce a five to seven milligram per dl increase in cholesterol levels. You might think that's not very much, but when you consider that for every milligram of increase in cholesterol level there's about a one percent increase in risk for coronary heart disease, then we could attribute five to seven percent of all coronary heart disease to trans-fatty acids in the diet. (emphasis supplied). In May 1994, Drs. Walter Willett and Albert Ascherio, members of the Harvard University Department of Nutrition and Epidemiology, reviewed the growing science on trans fatty acids and heart disease, and concluded:[xxvii] Although the percentage of coronary heart disease deaths in the United States attributable to intake of trans fatty acids is uncertain, even the lower estimates from the effects on blood lipids would suggest that more than 30,000 deaths per year may be due to consumption of partially hydrogenated vegetable fat. Furthermore, the number of attributable cases of nonfatal coronary heart disease will be even larger. Drs. Willett and Ascherio also concluded (p. 723) that trans fatty acids reduce protective HDL cholesterol,[xxviii] and increase lipoprotein Lp(a), a potent indicator of cardiovascular risks.[xxix] They recommended (p. 724) “a regulated phaseout or strict limitation of partially hydrogenated fat in the U.S. diet.”[xxx] In April 1995, at a symposium in San Diego sponsored by the American Society for Clinical Nutrition, Professor Martijn Katan of Wageningen Agricultural University in the Netherlands argued that available scientific evidence justifies eliminating trans fatty acids from margarine, or at least labeling them as saturates. Professor Katan proposed manufacturing a trans-free margarine containing 10%-15% tropical oils. Due to health concerns, Canadian and some European public health authorities also have taken action against trans fatty acids. Canadian health authorities required labels on special dietary foods to declare trans fatty acid content as well as saturated fatty acid content.[xxxi] In addition, Canada will require food manufacturers to disclose trans fat content of all foods in December, 2005.[xxxii] English health authorities recommended that trans fatty acids be “regarded as equivalent” to cholesterol-raising types of saturated fatty acids. [xxxiii] Public health officials in the Netherlands are committed to removing trans fatty acids from the marketplace.[xxxiv] In sum, palm oil is a healthful and versatile product used in many of America's favorite foods. Americans rarely use palm oil to cook with themselves. However, products made with palm oil – including baked goods and noodle soups – have a positive role to play in a healthful, balanced diet, particularly when compared to products containing partially hydrogenated fats.
[i] Excerpted from speech on food labeling policy given at the Journalists' Conference, Washington, D.C. (Dec. 1, 1988). [ii] Letter from James C. Simmons, District Director, Cincinnati District to Joseph Pichler, President/CEO, The Kroger Company (Nov. 13, 1991). [iii] Letter from John H. Turner, Director, Atlanta District to Ron E. Doggett, President, Goodmark Foods, Inc. (Feb. 3, 1992). [iv] Elson, “Tropical Oils: Nutritional and Scientific Issues,” 31 Crit. Rev. Food Sci. & Nutr. 79 (1992); “New Findings on Palm Oil,” 45 Nutr. Rev. 205 (1987). [v] Bonanome & Grundy, “Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels,” 318 New Eng. J. Med. 1244 (1988); Grundy, “Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol,” 314 New Eng. J. Med. 745 (1986); Mattson & Grundy, “Comparison of effects of dietary saturated, monounsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man,” 26 J. Lipid Res. 194 (1985); Baudet, et al., “Modification in the composition and metabolic properties of human low density and high density lipoproteins by different dietary fats,” 25 J. Lipid Res. 456 (1984); Anderson & Grande, “Independence of the effects of cholesterol and degree of saturation of the fat in the diet on serum cholesterol in man,” 29 Am. J. Clin. Nutr. 1184 (1976); Ahrens, et al., “The influence of dietary fats on serum-lipid levels in man,” The Lancet 943 (1957); Khan, et al., “Comparative physiological evaluation of palm oil and hydrogenated vegetable oils in Pakistan,” National Conf. on Oil Palm/Palm Oil, Kuala Lumpur (Oct. 11, 1989); Lim, et al., “Hypocholesterolemic effects of a palm oil diet on human volunteers in Malaysia,” National Conf. on Oil Palm/Palm Oil, Kuala Lumpur (Oct. 11, 1989). [vi] “Palm Oil: A Compilation of Documented Facts on Nutritional Effects of Palm Oil,” Palm Oil Research Institute of Malaysia, 1, 3 (Feb. 1989). The scientists included Charles Elson of the University of Wisconsin, Madison, Roslyn B. Alfin-Slater of UCLA, David Kritchevsky of the Wistar Institute, David Klurfeld of Wayne State University and Randall Wood of Texas A&M University. [vii] Ng, et al., “Dietary palmitic acid (16:0) and oleic acid (18:0) exert similar effects on serum cholesterol and lipoprotein profiles in normocholesterolemic humans,” 11 J. Am. Coll. Nutr. 383 (1992) (olive oil); Hornstra, et al., “A palm oil-enriched diet lowers serum lipoprotein(a) in normocholesterolemic volunteers,” 90 Atherosclerosis 91 (1991) (palm oil diet results in significant reduction of lipoprotein(a) as compared to habitual diet); Marzuki, et al., "Influence of dietary fat on plasma lipid profiles of Malaysian adolescents,” 53 Am. J. Clin. Nutr. 1010S (1991) (serum lipid and lipoprotein profiles resulting from palm oil diet compare favorably to those resulting from soybean oil diet); Ng, et al., “Nonhypercholesterolemic effects of a palm olein diet in Malaysian volunteers,” 53 Am. J. Clin. Nutr. 1015S (1991) (corn oil and palm olein diets lowered total cholesterol and LDL/HDL from baseline values, with corn oil causing greater reductions); see also Driss, “Nutritional role of dietary fats: special reference to palm oil,” 45 Oleagineux 384 (1990) (concluding from Dutch, Malaysian, Pakistani and Korean studies that palm oil does not behave like saturated animal fat, but is neutral or cholesterol-lowering); Wood, et al., “Effect of palm oil and other dietary fats on serum lipids and lipoproteins: a human study,” abstracted in 1991 PORIM International Palm Oil Conference, 153 (Sept. 1991) (refined palm oil significantly increases HDL cholesterol and decreases apolipoprotein B); Hornstra & Sundram, “Influence of dietary palm oil on cardiovascular risk factors: a human study,” abstracted in 1991 PORIM International Palm Oil Conference, 154 (Sept. 1991) (palm oil diet significantly reduces LDL/HDL ratio, increases serum apolipoprotein A1, and decreases apolipoprotein B, as compared to habitual diet). [viii] Choudhury, et al., “Comparison of palmolein and olive oil: effects on plasma lipids and vitamin E in young adults,” 61 Am. J. Clin. Nutr. 1043 (1995). [ix] Animal studies have found that lauric and myristic acids, not palmitic acid, are primarily responsible for elevating serum cholesterol levels, at least in diets that are cholesterol free or low-cholesterol (i.e., less than 300 mg. per day human-equivalent), and contain modest percentages of fat and ratios of polyunsaturates to saturates in the range of normal diets. Hayes, et al., “Dietary saturated fatty acids (12:0, 14:0, 16:0) differ in their impact on plasma cholesterol and lipoproteins in nonhuman primates,” 53 Am. J. Clin. Nutr. 491 (1991) (monkeys); Lindsey, et al., “Dietary palmitic acid (16:0) enhances HDL cholesterol and LDL receptor mRNA abundance in hamsters,” 195 Proc. Soc. Exp. Biol. Med. 261 (1990); Hayes & Khosla, “Palm oil fatty acids (palmitate, oleate) have a neutral effect on plasma cholesterol in normo-cholesterolemic monkeys,” 55 Am. J. Clin. Nutr. 51 (1992). These findings have been corroborated in human studies. Ng, et al., “Dietary palmitic acid (16:0) and oleic acid (18:0) exert similar effects on serum cholesterol and lipoprotein profiles in normocholesterolemic humans,” 11 J. Am. Coll. Nutr. 383 (1992); Sundram, et al., “Palmitic acid is neutral relative to lauric and myristic acids in its effects on serum cholesterol in man,” 11 Arteriosclerosis Thrombosis 1614 (1991). [x] Grundy, “Influence Of Stearic Acid On Cholesterol Metabolism Relative To Other Long-Chain Fatty Acids,” 60 Am. Jur. Clin. Nutr. 986S (1994 supp.). See also Woollett & Dietschy, “Effect Of Long-Chain Fatty Acids On Low-Density-Lipoprotein-Cholesterol Metabolism,” 60 Am. Jur. Clin. Nutr. 991S (1994 supp.) (stearic acid biologically inactive and does not change LDL-cholesterol concentration); Kritchevsky, “Stearic Acid Metabolism And Atherogenesis: History,” 60 Am. Jur. Clin. Nutr. 997S (1994 supp.) (noting animal studies finding that stearic acid is less cholesterolemic than saturated fatty acids of shorter chain length). Before these studies appeared, FDA observed that, for stearic acid, “there is not clear evidence of risk relative to serum cholesterol.” Food Labeling; Mandatory Status of Nutrition Labeling and Nutrient Content Revision, 55 Fed. Reg. 29,487, 29,495 (July 19, 1990). [xi] Khosla & Hayes, “Dietary fat saturation in rhesus monkeys affects LDL concentrations by modulating the independent production of LDL apolipoprotein B,” 1083 Biochimica et Biophysica Acta 46 (1991); Lindsey, et al., “Dietary palmatic acid (16:0) enhances high density lipoprotein cholesterol and low density lipoprotein receptor mRNA abundance in hamsters,” 195 Proc. Soc. Exp. Biol. Med. 261 (1990); Hayes, et al., “Dietary 18:1/18:2 ratio correlates highly with hepatic FC and mRNas for apo A1, apo E, and the LDL receptor,” 78 Circulation 96 (supp. 1988). [xii] Qureshi, et al., “Response of hypercholesterolemic subjects to administration of tocotrienols,” 30 Lipid 1171 (1995); Kooyenga, et al., “Palm oil antioxidant effects in patients with hyperlipidaemia and carotid stenosis – 2 year experience,” 6 Asia Pacific J. Clin. Nutr. 72 (1997); see also Serbinova, et al., “Free radical recycling and intramembrane mobility in the anti-oxidant properties of alpha-tocopherol and alpha-tocotrienol,” 10 Free Radical Bio. & Med. 263 (1991); Qureshi, et al., “Dietary tocotrienols reduce concentrations of plasma cholesterol, apolipoprotein B, thromboxane B2, and platelet factor 4 in pigs with inherited hyperlipidemias,” 53 Am. J. Clin. Nutr. 1042S (1991); Qureshi, et al., “The structure of an inhibitor of cholesterol biosynthesis isolated from barley,” 261 J. Bio. Chem. 10544 (1986). At least one human study suggests tocotrienols reduce serum cholesterol levels. Qureshi, et al., “Lowering of Serum Cholesterol in Hypercholesterolemic Humans by Tocotrienols (Palmvitee),” 53 Am. J. Clin. Nutr. 1021S (1991); Gey, et al., “Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology,” 53 Am. J. Clin. Nutr. 326S (1991) (vitamin E plays a protective role against heart disease in human populations). [xiii] Hussein, et al., “Effect of dietary palm oil and its minor components on dimethyl-hydrazine (DMH) induced colon cancer in rats,” PIPOC 255 (1999); Nesaretnam, et al., “The effect of vitamin E tocotrienols from palm oil on chemically-induced mammary carcinogenesis in female rats,” 12 Nutr. Res. 63 (1992); Sundram, et al., “Effect of dietary palm oils on mammary carcinogenises in female rats induced by 7,12 dimethyl-benz(a)anthracene,” 49 Cancer Res. 1447 (1989) (palm oil exhibits protective effect in rat model of mammary cancer); Sylvester, et al., “Comparative effects of different animal and vegetable fats fed before and during carcinogen administration on mammary tumorigenesis, sexual maturation and endocrine function in rats,” 46 Cancer Res. 757 (1986). [xiv] Hornstra, “Dietary lipids and cardiovascular disease: effects of palm oil,” 43 Oleagineux 75 (1988) (palm oil exhibits anti-clotting properties in rat model); Rand, et al., “Effects of dietary palm oil on arterial thrombosis platelet responses and platelet membrane fluidity in rats,” 23 Lipids 1019 (1988). [xv] Nesaretnam, “Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status,” 33 Lipids 461 (1998); Elson, “Tropical Oils: Nutritional and Scientific Issues,” 31 Crit. Rev. Food Sci. & Nutr. 79 (1992); Cottrell, “Introduction: nutritional aspects of palm oil,” 53 Am. J. Clin. Nutr. 989S (1991). [xvi] Guthrie, et al., “Palm oil tocotrienols and plant flavonoids act synergistically with each other and with tamoxifen in inhibiting proliferation and growth of estrogen receptor-negative MDA-MB-435 and –positive MCF-7 human breast cancer cells in culture,” 6 Asia Pacific J. Clin. Nutr. 41 (1997). [xvii] Industrially processed vegetable oils are the major source of trans fatty isomers in the American diet. Trans fatty acids are present primarily in margarines and shortenings. A study published in 1993 concluded that 9.58 grams/day of trans fatty acids are ingested in an average American diet, which translates into 5% of total energy intake and 6% or more of total U.S. fat consumption. Litin & Sacks, “Trans fatty acid content of common foods,” 329 N. Engl. J. Med. 1969 (1993). This estimate is consistent with, and higher than, previous estimates ranging from 7.6 grams/day to 15.2 grams/day. Hunter & Applewhite, “Reassessment of trans fatty acid availability in the US. diet,” 54 Am. J. Clin. Nutr. 363 (1991); Chen, et al., “Trans fatty acids in Canadian human milk," 30 Lipids 15 (1995) (similar values obtained by direct analyses of human adipose tissue samples). Many Americans appear to consume substantially higher quantities. One study found average consumption of 27 grams/day in some subpopulations, which is roughly 24% of total fat intake. Enig, et al., “Isomeric trans fatty acids in the U.S. diet,” 9 J. Am. Coll. Nutr. 471 (1990). [xviii] “Labeling of Meat Food Products To Reflect the Inclusion of Imitation or Alternate Cheese; and the Effects of Consumption of Tropical Oils on the Soybean Program; Joint Hearing Before the Subcomm. on Livestock, Dairy and Poultry and the Subcomm. on Wheat, Soybeans and Feed Grains of the House Comm. on Agriculture,” 100th Cong., 1st Sess. at 131 (1988). [xix] Excerpted from speech on food labeling policy given at the Journalists' Conference, Washington, D.C. (Dec. 1, 1988). [xx] “Food Labeling: Trans Fatty Acids in Nutrition Labeling, Nutrient Content Claims, and Health Claims,” Proposed Rule, 64 Fed. Reg. 62,746 (Nov. 17, 1999). [xxi] 64 Fed. Reg. at 62,754. As early as January 1993, FDA acknowledged that scientific evidence suggests that trans fatty acids increase harmful LDL-cholesterol. “Food Labeling: Health Claims and Label Statements; Dietary Saturated Fat and Cholesterol and Coronary Heart Disease,” Final Rule, 58 Fed. Reg. 2739, 2745 (Jan. 6, 1993). Most evidence indicates that consumption of trans fatty acids has increased during this century, and is increasing. Recently, in response to recommendations by public health authorities to decrease saturated fat consumption, Americans have turned away from dairy products such as butter towards margarine. Fast food chains are switching from beef tallow, a saturated animal fat (3-5% natural trans content), to partially hydrogenated (35% average trans) vegetable oils. French-fried potatoes prepared in this fashion would have 25-35% of their total fatty acid content of the trans variety. [xxii] Food Labeling: Trans Fatty Acids in Nutrition Labeling, Nutrient Content Claims, and Health Claims, 68 Fed. Reg. 41,433 (July 11, 2003) (Trans Fatty Acids in Nutrition Labeling). [xxiii] Although the health impacts of trans fatty acids were little studied until the 1990s, there has long been serious concern that that trans fatty acids have the same effect on blood cholesterol as certain saturates. “The Health Aspects of Trans-Fatty Acids,” Life Sciences Research Office, Federation of American Societies for Experimental Biology (1985); Report of the Ad Hoc Committee on the Composition of Special Margarines, Canadian Ministry of Supply and Services (1980). [xxiv] Grundy, “Trans monounsaturated fatty acids and serum cholesterol levels,” 323 New Eng. J. Med. 480 (1990). [xxv] Mensink & Katan, “Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects,” 323 New Eng. J. Med. 439 (1990). [xxvi] Transcript, “Should the Recommended Dietary Allowances (RDAs) Be Revised?,” Workshop and Public Hearing, The Food and Nutrition Board, Institute of Medicine, National Academy of Sciences, Session 3, p. 163 (June 28, 1993) (emphasis supplied). [xxvii] Willett & Ascherio, “Trans Fatty Acids: Are the Effects Only Marginal?,” 84 Am. J. Pub. Health 722 (1994). [xxviii] Other studies confirm this conclusion. Wood, et al., “Effect of Butter, Mono- and Polyunsaturated Fatty Acid-Enriched Butter, Trans Fatty Acid Margarine, and Zero Trans Fatty Acid Margarine on Serum Lipids and Lipoproteins in Healthy Men,” 34 J. Lipid Res. 1 (1993); Judd, et al., “Dietary Trans Fatty Acids: Effects on Plasma Lipids and Lipoproteins of Healthy Men and Women,” 59 Am. J. Clin. Nutr. 861 (1994); Zock & Katan, “Hydrogenation Alternatives: Effects of Trans Fatty Acids and Stearic Acid Versus Linoleic Acid on Serum Lipids and Lipoproteins in Humans,” 33 J. Lipid Res. 399 (1992); Nestel, et al., “Plasma Lipoprotein Lipid and Lp[a] Changes with Substitution of Elaidic Acid for Oleic Acid in the Diet,” 33 J. Lipid Res. 1029 (1992); Mensink & Katan, “Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects,” 323 New Eng. J. Med. 439 (1990). [xxix] Mensink, et al., “Effect of Dietary Cis and Trans Fatty Acids on Serum Lipoprotein[a] Levels in Humans,” 33 J. Lipid Res. 1493 (1992). [xxx] Trans fatty acids also may hinder healthy prenatal and infant development. Simpopoulos, et al., “The 1st Congress of the International Society for the Study of Fatty Acids and Lipids (ISSFAL): Fatty Acids and Lipids from Cell Biology to Human Disease. Report of a Conference.” 35 J. Lipid Res. 169 (1994) (questioning “the safety of a high dietary supply of trans fatty acids in the perinatal period”). [xxxi] Health Protection and Food Laws, Minister of National Health and Welfare (Canada 1987). [xxxiii] “Diet And Cardiovascular Disease,” Department of Health and Social Security, Committee on Medical Aspects of Food Policy, Report of the Panel on Diet in Relation to Cardiovascular Disease, 5,6,9 (London 1984). [xxxiv] Katan, “Exit trans fatty acids,” 346 Lancet 1245 (1995). |
The Truth About Palm Oil *Landmark Article 
