Earlier work has shown that increasing concentration of palmitic acid at the sn-2 position of a fat enhances the atherogenic properties of that fat. This effect has been observed with lard, tallow, cottonseed oil, and palm oil. In the experiment reported here, we have studied the atherogenic effects of four synthetic fats fed to rabbits as 58% (w/w) of the total fat (15%) (w/w) of a semipurified diet containing 0.05% cholesterol. The fats being tested were: 1,3-stearoyl-2-oleoylglycerol (SOS); 1,2-stearoyl-3-oleoylglycerol (SSO); 1,3-palmitoyl-2-oleoylglycerol (POP); and 1,2-palmitoyl-3-oleoylglycerol (PPO). After 20 wk on diet there were no differences among the groups in weight gain, liver weight, serum, or liver lipids. These data are consistent with our previous findings. There were significant differences in atherosclerosis. The most severe atherosclerosis was observed in group PPO and the least in groups SSO and POP. Severity of atherosclerosis was graded visually on a 0-4 scale. The average atherosclerosis [(aortic arch and thoracic aorta) divided by 2] was: SOS--1.35; SSO--0.97; POP--0.83; and PPO--1.80. Fecal fat excretion (an indicator of fat absorption) was higher in the two groups fed the stearic acid-rich fats and lower in groups fed the palmitic acid-rich fats. There were no differences in low density lipoprotein particle size. The results confirm previous findings concerning the increased atherogenicity of fats bearing palmitic acid at the sn-2 position. The mechanism underlying these observations is moot but may, in part, reflect greater absorption of the atherogenic fat.

We have compared the effects of three different margarines, one based on palm oil (PALM-margarine), one based on partially hydrogenated soybean oil (TRANS-margarine) and one with a high content of polyunsaturated fatty acids (PUFA-margarine), on serum lipids in 27 young women. The main purpose of the study was to test if replacement of trans fatty acids in margarine by palmitic acid results in unfavorable effects on serum lipids. The sum of saturated fatty acids (12:0, 14:0, 16:0) was 36.3% of total fatty acids in the PALM-diet, the same as the sum of saturated (12:0, 14:0, 16:0) (12.5%) and trans (23.1%) fatty acids in the TRANS-diet. This sum was 20.7% in the PUFA-diet. The content of oleic acid was 37.9, 35.2, and 38.6%, respectively, in the three diets, whereas linoleic acid amounted to 16, 13.5, and 27.3%, respectively. Total fat provided 30-31% and the test margarines 26% of total energy in all three diets. The subjects consumed each of the diets for 17 d in a Latin-square crossover design. There were no significant differences in total cholesterol, low density lipoprotein (LDL)-cholesterol and apolipoprotein B (apoB) between the TRANS- and the PALM-diets. High density lipoprotein (HDL)-cholesterol and apoA-1 were significantly higher on the PALM-diet compared to the TRANS-diet whereas the ratio of LDL-cholesterol to HDL-cholesterol was lower, although not significantly (P = 0.077) on the PALM-diet. Total cholesterol, LDL-cholesterol, and apoB were significantly lower on the PUFA-diet compared to the two other diets. HDL-cholesterol was not different on the PALM- and the PUFA-diets but it was significantly lower on the TRANS-diet compared to the PUFA diet. Compared to the PUFA-diet the ratio of LDL- to HDL-cholesterol was higher on both the PALM- and the TRANS-diets whereas apoA-1 was not different. Triglycerides and lipoprotein (a) were not significantly different among the three diets. We concluded that nutritionally, palmitic acid from palm oil may be a reasonable alternative to trans fatty acids from partially hydrogenated soybean oil in margarine if the aim is to avoid trans fatty acids. A palm oil-based margarine is, however, less favorable than one based on a more polyunsaturated vegetable oil.

We previously found no difference in healthy young adults' plasma cholesterols between palmolein and olive oil as the major dietary lipid, although the former is high in palmitic acid (16:0) but the latter in oleic acid (18:1 cis). In the experiment reported here we compared the effects of palmolein against another monounsaturated oil, highly oleic sunflower oil (HOSO), on plasma cholesterol in both young and middle-aged healthy adults. The test oils were provided as frying oil of potato crisps (150 g/day in men; 100 g/day in women) against low-fat background diets in free-living motivated volunteers. The design was a randomised double-blind 4-week/3-week crossover trial. Compliance was monitored with continuous dietary diaries and by measuring (fasting) plasma lipid fatty-acid pattern. Plasma lipids and vitamin-E compounds were measured at the start and twice at the end of each test period. In combined young plus older subjects (n = 42) mean plasma total and low-density-lipoprotein cholesterol (LDL-c) values were both 7% (significantly) lower on HOSO than on palmolein, but because high-density-lipoprotein cholesterol (HDL-c) was also 5% lower, the LDL-c/HDL-c ratio was only 3% lower on HOSO than on palmolein. The difference between the present results with HOSO and previous results with olive oil both compared against palmolein suggest that olive oil is associated with higher plasma cholesterols than other monounsaturated oils. In both the young and older subgroup, LDL-c was lower on HOSO but because HDL-c moved down too in the young subgroup, the LDL-c/HDL-c ratio was lower on HOSO only in the older subjects. Palmolein has an unusual pattern of E vitamins, with a high content of tocotrienols, notably the gamma-isomer. Unlike alpha-tocopherol however, there was no sign of these tocotrienols in subjects' plasmas.

The cholesterol-raising effect of dietary saturated fatty acids is largely accounted for by lauric, myristic, and palmitic acids. Dairy fat is a major source of myristic acid, and palm oil is especially rich in palmitic acid. Myristic acid is suspected of being much more cholesterolemic than palmitic acid, but direct comparisons have been lacking. We therefore fed 36 women and 23 men three diets that differed from each other in palmitic, oleic, and myristic acid content by about 10% of total energy. We used palm oil, high-oleic acid sunflower oil, and a specially produced high-myristic acid fat to achieve these differences. Each diet was consumed for 3 weeks in random order. Mean serum cholesterol was 4.53 mmol/L on the high-oleic acid diet, 4.96 mmol/L on the palmitic acid diet, and 5.19 mmol/L on the myristic acid diet (P < .0001 for all comparisons). Myristic acid raised low-density lipoprotein (LDL) cholesterol by 0.11 mmol/L, high-density lipoprotein (HDL) cholesterol by 0.12 mmol/L, and apolipoprotein (apo) A-I by 7.2 mg/dL relative to palmitic acid; increases relative to oleic acid were 0.50 mmol/L for LDL cholesterol, 0.15 mmol/L for HDL cholesterol, 6.0 mg/dL for apoB, and 8.9 mg/dL for apoA-I (P < .01 for all comparisons). The HDL cholesterol and apoA-I levels on the palmitic and oleic acid diets were the same. None of the responses differed significantly between woman and men. Myristic acid and palmitic acid both caused high LDL cholesterol and apoB levels and low HDL to LDL ratios.

Twenty-one healthy normocholesterolemic young adults, men and women, completed a randomized 30-d/30-d crossover comparison of the effect of palmolein and olive oil on plasma lipids. The subjects were free-living volunteers who changed to low-fat diets to which one of the test oils was added (used as a spread, for baking, or for frying) in turn. Complete food records were kept throughout: the test oils were compared at 17% of total dietary energy. Under the conditions of this experiment plasma total and low-density-lipoprotein (LDL) cholesterol were almost identical with the two oils, so that when the palmitic acid (16:0) in palm oil replaced oleic acid (18:1) in olive oil the expected increase in LDL cholesterol was not seen. These results indicate that 16:0, though saturated, is not always a plasma cholesterol-raising fatty acid. Palmolein is rich in vitamin E, alpha-tocopherol, and especially tocotrienols, but the latter were barely detectable in plasma.

Thirty-eight male volunteers participated in a double-blind cross-over trial evaluating the effect of replacing the usual sources of saturated fat in the Dutch diet (animal fats and hydrogenated oils) by palm oil, which is virtually free of cholesterol and trans-fatty acids, on serum lipids, lipoproteins and apolipoproteins. Maximum (about 70%) replacement had no significant effect on serum total cholesterol or most lipoprotein fractions, but resulted in an 11% increase in serum high-density-lipoprotein (HDL)2-cholesterol relative to the control (P2 = 0.01). The palm-oil diet also caused an 8% decrease in low-density-lipoprotein (LDL):HDL2 + HDL3-cholesterol ratio (P2 = 0.02) as well as a 9% decrease in triacylglycerols in the low-density-lipoprotein fractions (P2 = 0.01). Palm oil consumption resulted in a 4% increase in serum apolipoprotein AI (P2 = 0.008) and a 4% decrease in apolipoprotein B (P2 = 0.01) relative to the control diet; the B:AI apolipoprotein ratio was decreased by 8% (P2 < 0.0001). These results were not significantly affected by the different lipoprotein E phenotypes of the volunteers. Although the observed differences were relatively modest, the present study, nonetheless, indicates that dietary palm oil, when replacing a major part of the normal fat content in a Dutch diet, may slightly reduce the lipoprotein- and apolipoprotein-associated cardiovascular risk profiles.

Cebus and rhesus monkeys were fed cholesterol-free diets providing 40% of energy as fat for 6-wk periods. The fats were high-linoleic acid safflower oil (HLSO), high-oleic acid safflower oil (HOSO), or palm oil (PO), rich in polyunsaturated (18:2), monounsaturated (18:1), or saturated (16:0) fatty acids, respectively. In cebus monkeys, plasma cholesterol concentrations during HLSO intake were 17-19% lower than those during HOSO or PO intake, attributed to a decrease in high-density lipoprotein (HDL). Plasma triglyceride (TG) and low-density-lipoprotein (LDL) cholesterol concentrations were comparable during all dietary treatments. Sixty-eight percent of total LDL catabolism was receptor mediated in all dietary groups and this was associated with similar apolipoprotein B pool sizes and fractional catabolic rates. Rhesus monkeys revealed similar cholesterol concentrations (total, LDL, and HDL) during all dietary treatments. TG concentrations during PO intake were 34% and 63% higher than those during HOSO and HLSO intakes, respectively. Hence, dietary 16:0 and 18:1 produce similar effects on LDL and HDL metabolism in normocholesterolemic primates.

Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.

In a recent study from this laboratory, rhesus monkeys fed a 90% palm oil/10% soybean oil-containing diet (PS), rich in 16:0 and 18:1 fatty acids, had decreased total and LDL cholesterol concentrations compared to monkeys fed a 90% coconut oil/10% soybean oil-containing diet (CS), rich in 12:0 and 14:0 fatty acids. To investigate the metabolic basis of these changes, homologous 125I-VLDL and 131I-LDL were injected simultaneously into eight monkeys (four per dietary group). Analysis of apo B specific activity curves revealed that PS monkeys had an increased pool size of VLDL apo B (P less than 0.02), a 3-fold increase in the total VLDL apo B transport rate (P less than 0.001), a decreased pool size of LDL apo B (P less than 0.01) and a 2-fold decrease in the total transport rate of LDL apo B (P less than 0.001), while the irreversible FCR for VLDL apo B and LDL apo B was similar between dietary groups. PS monkeys derived a greater percentage of LDL apo B from VLDL catabolism resulting in a greater transport rate of LDL apo B from VLDL catabolism (P less than 0.055), in comparison to CS monkeys. For CS monkeys the proportion as well as the amount of LDL apo B derived from VLDL-independent catabolism (i.e., LDL apo B derived from sources other than VLDL catabolism) was higher (P less than 0.001) than the values obtained in PS monkeys. In both dietary groups the proportion of VLDL apo B converted to LDL apo B was similar, although the absolute amount was higher for the PS monkeys (P less than 0.06). The proportion of VLDL apo B directly removed from the circulation was similar for both dietary groups, with the absolute amount being higher for the PS monkeys (P less than 0.001). Consistent with the lower pool size of LDL apo B and the higher pool size of VLDL apo B observed in PS monkeys, plasma and LDL cholesterol concentrations tended to be lower, whereas plasma triacylglycerol and VLDL cholesterol concentrations tended to be higher, but these changes were not statistically significant. Although total apo B and VLDL apo B transport rates were increased 2-3-fold in PS monkeys, LDL apo B concentration was reduced by 40% (P less than 0.02) attributed to a significant reduction in the mass and proportion of LDL apo B derived independent of VLDL catabolism.

The effects on serum lipids of diets prepared with palm olein, corn oil, and coconut oil supplying approximately 75% of the fat calories were compared in three matched groups of healthy volunteers (61 males, 22 females, aged 20-34 y). Group I received a coconut-palm-coconut dietary sequence; group II, coconut-corn-coconut; and group III, coconut oil during all three 5-wk dietary periods. Compared with entry-level values, coconut oil raised the serum total cholesterol concentration greater than 10% in all three groups. Subsequent feeding of palm olein or corn oil significantly reduced the total cholesterol (-19%, -36%), the LDL cholesterol (-20%, -42%%) and the HDL cholesterol (-20%, -26%) concentrations, respectively. Whereas the entry level of the ratio of LDL to HDL was not appreciably altered by coconut oil, this ratio was decreased 8% by palm olein and 25% by corn oil. Serum triglycerides were unaffected during the palm-olein period but were significantly reduced during the corn-oil period.