|
Pulp Fiction: Palm Oil and Heart Health |
|
|
|
Written by Frank Tate
|
 Much has been written and said about palm oil ever since the dubious Center for Science in the Public Interest (CSPI) launched their questionable campaign against palm oil alleging that it was damaging to heart health.
The Palm Oil Truth Foundation takes the view that CSPI’s campaign against palm oil is both misguided and mischievous. At the very least, their position against palm oil cannot withstand the scrutiny of scientific and factual examination.
Let us examine the science and the facts and in the process get rid of some the more popular misconceptions and myths on palm oil perpetuated by the likes of CSPI.
First, palm oil is a vegetable oil and since it is not an animal or dairy product, it does not contain any cholesterol. Secondly, palm oil is not palm kernel oil. It is produced from the pulp of the mesocarp of the palm oil fruit. Next, palm oil contains much less saturated fat than palm kernel oil or even coconut oil.
Attacking palm oil as being “saturated,” because it contains 44% palmitic acid and 5% stearic acid, CSPI alleged that palm oil 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.” (i)
Many pre-1990 human feeding studies reported that palm oil diets resulted in lower serum cholesterol levels than pre-study values. (ii) 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.” (iii) 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.(iv) 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. (v) 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, (vi) and stearic (10%), which also does not raise blood cholesterol concentrations. (vii) Animal studies have found that palm oil stimulates synthesis of protective HDL cholesterol and removal of harmful LDL cholesterol. (viii) 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. (ix)
It also appears that palm oil, as compared to saturated fats and oils, may pose a lesser degree of risk of cancer, (x) or thrombosis.(xi). This may be due to tocotrienols (xii) or other phytonutrients (xiii) 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.
Finally, in 1991, the FDA began taking enforcement action against food manufacturers making “no palm oil” and “no tropical oils” label claims. The FDA issued warning letters to The Kroger Company (xiv) and Goodmark Foods, Inc., (xv) 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 the passage of the Nutrition Labeling and Education Act of 1994, the FDA issued regulations prohibiting claims such as “no palm oil” and “no tropical oils” from food labels, unless and until pre-approved by the FDA through a petition process. See 21 C.F.R. § 101.69. The 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 the FDA and will have to face the consequent penalties.
The Palm Oil Truth Foundation wonders whether the curiously named Center for Science in the Public Interest is even aware of these scientific and regulatory developments – or would they rather wish that the consumer continue to believe in their pulp fiction? Certainly not in this day and age! THE END.
References:
(i) 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).
(ii)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).
(iii) “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.
(iv) 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).
(v) 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).
(vi) 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).
(vii) 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).
(viii) 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).
(ix) 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).
(x) 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).
(xi) 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).
(xii) 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).
(xiii) 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).
(xiv) Letter from James C. Simmons, District Director, Cincinnati District to Joseph Pichler, President/CEO, The Kroger Company (Nov. 13, 1991).
(xv) Letter from John H. Turner, Director, Atlanta District to Ron E. Doggett, President, Goodmark Foods, Inc. (Feb. 3, 1992). |
Center for Science? More like Center for 'Seance' - you know the kind that gathers to communicate with the dead. That's how 'dead' the science in CSPI really is! Posted by Dennis Cook, on June 16, 2008 at 12:57
Yahoo! CSPI exposed and found out at last! Posted by D Yang, on June 16, 2008 at 12:48
Impressive article and references, made me realise palm oil is actually good for me. Posted by Hae Kyun, on June 16, 2008 at 4:32
Leave your comments
Please login to leave your comments.
|
Pulp Fiction: Palm Oil and Heart Health 
