PALM OIL NUTRITION UPDATE 2
Several human clinical trials have now evaluated palm oil's effects on blood lipids and lipoproteins. These studies suggest that palm oil and palm olein diets do not raise plasma TC and LDL-cholesterol levels to the extent expected from its fatty acid composition.
Palm Oil Nutrition Update 2:
Modulation of human lipids and lipoproteins by dietary palm oil and palm olein: a review KALYANA SUNDRAM
Palm Oil Research Institute of Malaysia (MPOB)
P.O. Box 10620, 50720 Kuala Lumpur
Several human clinical trials have now evaluated palm oil's effects on blood lipids and lipoproteins. These studies suggest that palm oil and palm olein diets do not raise plasma TC and LDL-cholesterol levels to the extent expected from its fatty acid composition. With maximum substitution of palm oil in a Western type diet some coronary heart disease risk factors were beneficially modulated: HDL2-cholesterol was significantly increased while the apolipoprotein B/A1 ratio was beneficially lowered by palm oil. Comparison of palm olein with a variety of monounsaturated edible oils including rapeseed, canola, and olive oils has shown that plasma and LDL-cholesterol were not elevated by palm olein. To focus these findings, specific fatty acid effects have been evaluated. Myristic acid may be the most potent cholesterol raising saturated fatty acid. Palmitic acid effects were largely comparable to the monounsaturated oleic acid in normolipemic subjects while trans fatty acids detrimentally increased plasm cholesterol, LDL-cholesterol, lipoprotein Lp(a) and lowered the beneficial HDL-cholesterol. Apart from these fatty acids there is evidence that the tocotrienols in palm oil products may have a hypocholesterolemic effect. This is mediated by the ability of the tocotrienols to suppress HMG-CoA reductase. These new findings on palm oil merit a scientific reexamination of the classical saturated fat-lipid hypothesis and its role in lipoprotein regulation.
Dietary fats (and fatty acids) are known to modulate plasma lipids and lipoproteins. This concept has been extensively researched upon since the early 1950s and evidence has steadily accumulated hypothesizing a positive correlation between saturated fat intake and increased levels of plasma total cholesterol (TC) in humans. The classical Keys and Hegsted equations (1,2) indicated that the three saturated fatty acids lauric, myristic and palmitic were equally cholesterol raising. Hegsted (3) originally showed that myristic acid was more cholesterolemic than palmitic acid in humans. Nevertheless, this conclusion was subsequently revised after a series of experiments with modified triglycerides. Thereafter, both investigators developed their own regression equations that predicted plasma cholesterol response on the basis of energy contributed by the sum of saturated and polyunsaturated fatty acids in one's diet. These equations assumed that the monounsaturates were neutral but that dietary cholesterol affected plasma cholesterol besides the fatty acids.
Resulting from these and other findings, there has been a tremendous effort to educate the consumer to choose fats containing fatty acids that could help maintain normal cholesterol levels. Such recommendations are embodied in almost every major national health report focused at reducing the incidence and mortality from coronary heart disease (CHD). Awareness of these recommendations by the consumers has been shown by a switch from animal saturated fats to polyunsaturated oils. Such changes are however related to the functionality of the oils and fats concerned. The replacement of butter with margarine and the trend towards the increased consumption of polyunsaturated margarines and other low saturates containing fat-rich products was seen as a positive stride in reducing CHD incidence. New data has now shown that hydrogenation of liquid polyunsaturated and monounsaturated oils used in such product formulations results in trans fatty acids that increase the lipid associated risk factors. Since palm oil contains 44% of its composition as saturated palmitic acid, it is generally assumed that TC elevation following its long term consumption would be imminent. Indeed several human studies (4-8) have reported that palmitic acid enriched diets derived from palm oil resulted in higher TC and low density lipoprotein cholesterol (LDL-C) than did diets enriched either in oleic or linoleic acids. However, newer studies to be examined below have since produced results that are contradictory to the above. At least one population (epidemiology) study has reported that normal TC values are possible in a dietary environment in which palm oil was the predominant fat source (9). The issue is further confounded by reported effects of triglyceride species (10) and the minor components (11) on cholesterol modulation.
Historical studies evaluating palm oil effects
One of earliest clinical trials evaluating palm oil was pioneered by Arhens et al. (12) who fed two of their subjects a liquid formula diet containing 40% energy as palm oil under metabolic conditions. The TC levels of both these subjects fed palm oil was significantly higher than during a corn oil period. Nevertheless, the TC values after the palm oil period was lower than the baseline values. Grande et al. (13) showed that a palm oil enriched diet resulted in higher TC than a diet predominated by stearic acid derived from cocoa butter. This study was also noteworthy in that it confirmed Key's earlier observation that stearic acid lacked a cholesterol raising effect.
Anderson et al. (4) fed 12 volunteers diets containing 35% saturated fat contributed by two parts of palm oil and one part coconut oil and compared its cholesterolemic effects with a polyunsaturated safflower oil diet. The safflower oil diet resulted in lower serum TC than the saturated fat diet. However, the saturated fat diets actually resulted in approximately 10% lower serum TC levels than the subjects' habitual diets. In 1984, Baudet et al. (5) undertook a dietary trial using Benedictine nuns to evaluate the effect of 30% fat calories contributed predominantly (two thirds) by palm oil, sunflowerseed oil, peanut oil or milk fat on serum lipid and lipoprotein levels. The sunflowerseed oil diet reduced serum TC and LDL-C significantly compared with all other diets. Serum TC and LDL-C were essentially similar after the palm oil and peanut oil diets whereas milk fat resulted in significantly higher TC and LDL-C levels than all the other test diets.
Mattson and Grundy (6) fed 20 male volunteers a liquid formula diet containing 40% calories contributed either by palm oil, high oleic safflower oil or high linoleic safflower oil. After four weeks, the high oleic and high linoleic safflower oil diets produced significantly lower TC and LDL-C than the palm oil diet. HDL-C on the palm oil and high oleic safflower oil diets were similar but HDL-C on the high linoleic safflower oil diet was significantly lower.
In a follow-up study, Grundy and Vega (7) fed 11 patients liquid formula diets containing 40% fat calories (high fat) and compared their effects with a 20% fat calories (low fat) diet. The high fat diets were formulated with either coconut oil, palm oil or high oleate safflower oil. The 11 patients were then subdivided into two groups in which seven were fed the coconut oil diet while the remaining four the palm oil diet. The patients were also rotated through the high-oleate safflower oil and low-fat diets. TC and LDL-C were significantly lower on the high oleate safflower oil diet compared with all other test diets. The four patients on the palm oil diet had TC, LDL-C and HDL-C values than were lower than the coconut oil diets and the habitual diets of these patients.