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Asia Pacific J Clin Nutr (1997) 6(1): 72-75

Palm oil antioxidant effects in patients with hyperlipidaemia and carotid stenosis-2 year experience

DK Kooyenga1 BS, M Geller2 MD, TR Watkins1 PhD, A Gapor4, E Diakoumakis3 MD, ML Bierenbaum1 MD

1Kenneth L. Jordan Research Group, Montclair, NJ, USA
2Department of Neurology, Elmhurst Medical Center, Queens, NY, USA
3Department of Radiology, Elmhurst Medical Center, Queens, NY, USA
4Palm Oil Research Institute of Malaysia, Kuala Lumpur, Malaysia

Antioxidants appear to play a role in the prevention of atherosclerosis. Here, we investigated the antioxidant properties of a g-tocotrienol and a-tocopherol enriched fraction of palm oil, in patients with carotid atherosclerosis. Serum lipids, fatty acid peroxides, platelet aggregation, and carotid artery stenosis were measured over a 24-month period in 50 patients with cerebrovascular disease. Change in stenosis was measured with bilateral duplex ultrasonography. These studies revealed apparent carotid atherosclerotic regression in eight and progression in two of the 25 antioxidant patients, while none of the control group exhibited regression and ten of 25 showed progression (P<0.01). Serum a-tocopherol doubled while tocotrienols were undetectable throughout the study. Serum thiobarbituric acid reactive substances, decreased in the treatment group from 1.08 ± 0.14 to 0.80 ± 0.14 mM (P<0.05) after 24 months, and in the placebo group, they increased nonsignificantly from 0.99 ± 0.16 to 1.06 ± 0.17 mM. Both antioxidant and placebo groups displayed significantly increased collagen-induced platelet aggregation responses (P<0.05) as compared with entry values. Serum total cholesterol, low density lipoprotein cholesterol, and triglyceride values remained unchanged in both groups, as did the plasma high density lipoprotein cholesterol values. Palm oil tocols appear to benefit the course of carotid atherosclerosis.


In recent years, evidence has linked processes involving oxygen-derived free radicals with the initiation and propagation of atherosclerosis. In particular, the oxidative modification of low density lipoproteins (LDL), with its ensuing sequelae of cytotoxic, thrombogenic, and chemotactic events, has emerged as a key step in promoting atherosclerosis1-3. Antioxidants, especially vitamin E, have received considerable attention as potential anti-atherogenic agents for over 40 years. A number of recent studies have demonstrated the ability of antioxidants to prevent ex vivo and in vitro LDL oxidation, and to potentially be able to amel-iorate the development of atherosclerotic lesions4-6. Epidem-iological studies have linked the dietary intake of vitamin E and other antioxidants with a reduced risk of coronary heart disease7,8, ischaemic heart disease9, ischaemic stroke10, coronary mortality11, and with a decrease in carotid artery wall thickness12. As the vitamin-rich distillate of palm oil [Palm Oil Research Institute of Malaysia (PORIM), Kuala Lumpur, Malaysia] is enriched with several antioxidant members of the vitamin E family (tocopherols and tocotrienols), it was felt worthwhile to investigate its antioxidant effects in patients with cerebrovascular disease.

Materials and methods

The study cohort consisted of 50 subjects (23 males and 27 females), ranging from 49-83 years of age, with carotid artery atherosclerosis as determined by duplex carotid ultrasonography. Eligibility criteria included subjects less that 85 years of age who had either had a hemispheric transient ischaemic attack, monocular blindness for less than 24 hours, or a nondisabling hemispheric stroke within the previous year. Subjects had carotid artery stenosis ranging from 15-79%. Subjects having stenosis beyond 79% were referred to surgery. Forty-four percent of placebo and 60% of test subjects had more than 49% stenosis of the carotid artery. All patients continued to receive their current medical care, including antihypertensive, antidiabetic, and anti-platelet (usually aspirin) treatment, except that 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors were discontinued.

At baseline, patients underwent standardised history, physical, and neurological examinations, an assessment of functional status, standardised laboratory tests, 12-lead electrocardiography, a chest X-ray, and duplex carotid ultrasonography. A synopsis of subject characteristics appear at baseline showing their similarity (Table 1; collagen-induced aggregation in ohms of resistance (W) was 16.9 for the antioxidant group, 17.7 for the placebo group; thrombin ATP release (mM) was 0.99 ± 0.46 and 1.02 ± 0.39 for the antioxidant and placebo groups, respectively).

Table 1. Comparison of patient characteristics at study entry by treatment group.

Patient Characteristic

Palm Vitee (n=25)

Placebo (n=25)






Gender (F/M)




Antiplatelet (aspirin) use (no.)




Anticoagulant use (no.)




Hypertensives (no.)




Diabetics (no.)




Abnormal EKGb (no.)




Abnormal chest X-rayb (no.)




Cigarette use (no.)




Height, inches (m)

64.8±4.2 (1.65±0.1)

64.4±3.5 (1.63±0.1)


Weight, lbs, (kg)

152.8±39.5 (69.4±17.9)

150.8±26.9 (68.6±12.2)


Systolic BP (mm Hg)




Diastolic BP (mm Hg)




No. > 49% carotid stenosis




Data expressed as means ± SEM; ns, not significant; (b) Abnormal for cardiovascular pathology; BP = blood pressure

Ultrasonography of the carotid arteries was done baseline and repeated at six and twelve months, and annually thereafter. Degree of stenosis was graded as: 0-15%; 16-49%; 50-79%, and 80-99%. Ultrasound duplex measurements were done with an Acuson 128 XP ultrasonograph (Acuson Co, Mountain View, CA) equipped with a 5 or 7 MHz transducer. The transducer aperture was 38 mm. Subjects were examined in the supine position. Change from one category to the next was reckoned regression or progression; a change of two categories was considered marked regression or progression. All ultrasound studies were done by the same person, who was unaware of treatment assignments and results of earlier measurements. The artery affecting neurological involvement was used for study in an attempt to more easily correlate the pathological and clinical changes.

Using a table of random numbers, patients were assigned to receive 300 mg capsules containing either 16 mg a-tocopherol, 40 mg g- and a-tocotrienols, and 240 mg palm superolein, or placebo (300 mg palm superolein). Palm superolein is a mixture of triglycerides with the predominant fatty acids being oleic, palmitic, and linoleic (6:4:1.51 ratio). The dosage of capsules containing placebo or palm oil antioxidants was 4 capsules daily. At the three- and six-month follow-up visits, the dosage was increased to 5 and 6 capsules daily, respectively, in an attempt to lower serum lipids. The dosage then remained at six capsules/day (96 mg a-tocopherol and 240 mg tocotrienol) for the remainder of the study. Patients were blinded throughout the trial; none in either group reported side effects. Investigators also were blinded about treatment groups, except for the one who distributed the capsules.

During the baseline, 3-, 6-, 9-, 12-, 18-, and 24-month visits venous blood was drawn after overnight fasting into EDTA and Vacutainer SST tubes (Becton Dickinson Co., Rutherford, NJ) with a sterile activator, stored at ambient temperature for five minutes, spun at ambient temperature at 3400 rpm, and either analysed immediately or stored frozen overnight before analysis. Though samples were identified during analysis, the analysis were done in a lab separate from the outpatient clinic. A lipid profile was measured in each subject to control for dietary changes or medicinal usage compliance which might have affected stenosis. It included serum total cholesterol, LDL cholesterol (by difference)13, and triglycerides for each visit using Reflotron methodology, which uses cholesterol esterase, oxidase, horse-radish peroxidase, and 3,3’ 5,5’-tetra-methylbenzidine dye, which is quantitated by reflectance (Boehringer-Mannheim, Indianapolis, IN) and high density lipoprotein (HDL) cholesterol using the same chemistry with EDTA-treated plasma. Triglycerides were quantitated by reaction with an esterase, glycerol kinase, glycerol phosphate oxidase, and peroxidase in the presence of a dye 4-(4-di-methylaminophenyl)-5-methly-2-(4-hydroxy-3,5-dimethyl-oxy-phenol)-imidazole-dihydrochloride. All analyses were done under amber light to reduce photooxidation. Fatty acid hydroperoxides were assayed according to Ohishi et al.14. Cumene hydroperoxide was used as the standard. The serum level of thiobarbituric acid reactive substances (TBARS) was measured to quantitate malon-dialdehyde equivalent materials by the method of Mihara et al.15. Serum levels of a-tocopherol were measured during baseline and at the 24-month visits by a high-performance liquid chromato-graphy method of Bieri et al.16 to monitor compliance. This method was not able to separate and detect measurable tocotrienols. Platelet aggregation in whole blood was measured with an impedance aggregometer (Chronolog Corp, Havertown, PA), using thrombin and collagen as agonists to initiate aggregation17, measuring only the primary wave of aggregation after the reaction had proceeded for six minutes. These measurements were made on a background of aspirin, as all subjects were taking aspirin during the trial.

Subject compliance was monitored by pill counts and measurement of serum vitamin levels, as indicated with each data panel. Pill counts showed 95% compliance for antioxidants.

Statistics were performed using Student’s t-test, the paired t-test, or the Mann-Whitney test. Available 3-, 6-, 9-, 12-, 18-, or 24-month data are presented.


Those patients being supplemented with tocopherol and tocotrienols for 24 months approximately doubled their serum a-tocopherol levels compared to baseline (Table 2). Serum levels of tocotrienol were below the detection limits of our high-performance liquid chromatography system; hence, no tocotrienol data are presented.

Table 2. Serum TBARS, LOPS, and a-tocopherol values and whole blood platelet responses of subjects given tocotrienols and tocopherol or placebo for 24 mona.

Palm oil fraction (tocotrienols)
Analyte Baseline 3 mon 6 mon 9 mon 12 mon 18 mon 24 mon
Collagen(W ) 16.9±2.4 14.6±2.6 9.52±1.7 15.6±2.2 12.0±1.8 13.2±2.9 25.5±3.0c
ATP(mM) 0.99±0.09 1.02±0.08 0.92±0.09 0.92±0.09 1.24±0.15 1.24±0.09 1.24±0.09
TBARS(mM) 1.08±0.14 0.66±0.10 0.68±0.11 0.68±0.11 0.80±0.11 1.24±0.22 0.80±0.14d
LOPS(mM) 1.73±0.15 1.58±0.20 4.52±1.3 4.1±1.1 3.6±1.5 2.6±0.60 2.85±0.55
Vit E(mM) 1.90±0.21 - - - - - 3.22±0.31e
Collagen(W ) 17.7±2.5 12.6±1.7 14.9±2.0 15.4±1.7 12.0±1.6 14.1±1.4 28.8±3.0f
ATP(mM) 1.02±0.08 0.97±0.10 0.99±0.14 1.00±0.13 1.04±0.15 0.91±0.08 0.91±0.08
TBARS(mM) 0.99±0.16 1.02±0.15 1.01±0.14 1.21±0.15 1.26±0.11 1.42±0.14 1.06±0.07
LOPS(mM) 2.27±0.23 1.58±0.20 2.1±0.32 6.7±3.14 3.6±1.90 2.8±0.70 3.02±0.62
Vit E(mM) 1.64±0.14 - - - -   1.19±0.14g

TBARS, thiobarbituric reactive substances; LOPS, fatty acid hydroperoxides. a, Data expressed as mean ± SEM. b, Thrombin agonist challenge, 1 NIH unit/mL. c, P<0.03 vs. respective baseline value. d, P<0.05 vs. respective baseline value. e, P<0.01 vs. respective baseline value. f, P<0.01 vs. respective baseline value. g, P<0.05 vs. respective baseline value.

Data of the effect of the palm oil antioxidants vs. placebo in lowering serum lipid oxidation products are shown (in Table 2). Patients receiving antioxidants attenuated their generation of TBARS after 24 months, with values decreasing from (mean ± SEM) 1.08 ± 0.14 to 0.80 ± 0.14 mM (P<0.05); whereas placebo subjects’ values showed no significant change (0.99 ± 0.16 to 1.06 ± 0.17 mM). At baseline, a difference was seen in hydroperoxide levels, possibly attributed to cigarette smoking (Table 1). Although not significant, the fatty acid hydroperoxides increased in both groups, rising from 1.73 ± 0.15 at baseline to 2.85 ± 0.55 mM after 24 months in the test group and 2.27 ± 0.23 to 3.02 ± 0.62 mM in the placebo group.

After 24 months, both antioxidant supplement (16.9 ± 2.4 W to 25.5 ± 3.0 W; P<0.03) and placebo (17.7 ±2.5 W to 28.8 ± 3.0 W; P<0.01) were associated with increase of collagen-induced platelet aggregation when compared with baseline. The platelet ATP response to thrombin did not change in the placebo group (1.02 ± 0.39 to 0.91 ± 0.42), but changed from 0.99 ± 0.46 to 1.24 ± 0.46 (nonsignificant) in the antioxidant group. Because both groups used aspirin, and aspirin usage was monitored carefully during the study, it appears that the increase seen in platelet aggregation resulted from a decreased adherence to prescribed aspirin intake.

The percentage change of carotid stenosis in patients by category differed in the groups receiving palm oil antioxidants and placebo after 24 months of treatment. The data indicated (Table 3) that seven (28%) of the subjects supplemented with antioxidants for 24 months moved one category to a lesser apparent degree of stenosis; one (4%) improved two categories, suggesting marked regression. Only two from this group (8%) exhibited progression of carotid atherosclerosis. The remaining 60% manifested no change in disease state. In contrast, 28%, of the placebo group appeared to progress, and 16% markedly progressed in carotid stenosis (P< 0.002; Mann-Whitney), while 56% of Doppler studies from the placebo group remained unchanged. No one receiving the placebo showed carotid plaque regression.

Table 3. Comparison of change in carotid stenosis in groups receiving tocotrienols and tocopherol or placebo for six and twenty-four monthsa.




6 months MR









  Total number



24 months MR









  Total number



a: Data expressed as number of subjects per category. MR, marked regression; K, regression; NC, no change; P, progression; MP, marked progression.

Treatment with the palm oil fraction (including 240 mg tocotrienols daily for 24 months) had no measurable effect on serum lipids (Table 4). Compared to baseline, serum total, LDL, HDL cholesterol, and triglyceride values remained virtually unchanged (non-significant) in test and in control groups over the observation periods.


Table 4. Response comparison of study groups to 24-mon antioxidant supplementation on serum cholesterol fractions and triglycerides.

Serum moiety (mM/L)








































































LDL-chol, low density lipoprotein cholesterol; HDL-chol, high density lipoprotein cholesterol. Data expressed as mean ± SEM; ns, not significant.
* Average molecular weight 914 daltons.


The purpose of the present clinical study was to test the effect of palm oil antioxidants in patients with carotid atherosclerosis. After extending the duration of the antioxidant supplementation study to 24 months, we found no measurable improvement in blood lipids, although we did observe an apparent improvement in blood flow in the carotid arteries of eight patients out of 25. Over a one-year period, in a population of hyper-cholesterolaemic Eastern Finnish men, an inverse correlation was observed between plasma anti-oxidant levels (vitamin E, b- carotene, selenium) and the increase in carotid intimal-media thickness18. Similarly, in both men and women, an inverse relationship was found between dietary antioxidant intake (a-tocopherol, ascorbic acid, b-carotene) and carotid artery wall thickness12.

To date, the precise mechanism(s) responsible for plaque regression have not been fully elucidated and appear to be complex and multifactorial. Earlier work from this laboratory documented the effective inhibition of platelet aggregation by antioxidants in hyperlipaemic patients19. After taking into account that one measure of the thrombogenicity of the blood was equally altered in both groups, and that the serum lipid profiles remained stable, it appears that the generation of serum TBARS data may provide a clue about the mode of action of palm oil antioxidants. Elegant studies aptly support the theory that antioxidants curtail the levels of blood lipid peroxides, and blunt the formation of atherosclerotic lesions. Esterbauer et al4 demonstrated vitamin E to be very effective in preventing in vitro oxidation of LDL, and Carew et al5 showed that the antioxidant probucol inhibited the progression of atherosclerotic lesions in LDL receptor-deficient rabbits.

Throughout this trial, we have observed no change in serum lipid levels. To the contrary, Qureshi et al20,21 have reported a reduction in both serum total and LDL cholesterol in human hyperlipidaemics and pigs supplemented with tocotrienol. Wahlqvist et al22, however, observed serum responses to both tocopherol and, to a lesser effect, tocotrienol supplementation in humans without any change in serum lipids. In preliminary trials with a rat model, we had observed a hypolipidemic effect with g-tocotrienol23; however, our results in rats were not confirmed by the outcome in patients on uncontrolled diets who were taking a variety of medications. From the present data, it appears that a decrease in serum cholesterol was not a prerequisite in the eight patients suggested to have reduced carotid atherosclerosis. This result is in contrast to coronary atherosclerosis, as we reported earlier24. Cholesterol is, indeed, a poor predictor of carotid, compared to coronary, plaque thickness. Miettenen et al25 have reported that although no significant decrease in coronary risk was measured when clofibrate was given with probucol, no stroke cases were observed in the 1200-subject study. Mao et al6 demonstrated that the attenuation of atherosclerotic lesions in Watanabe rabbits by a probucol analogue was not contingent on a concomitant reduction in the serum cholesterol levels. Similarly, probucol reduced the incidence of atherosclerotic lesions in a group of Japanese hypercholesterolaemic quail without altering the plasma total or lipoprotein cholesterol levels26. These investigators attributed this effect to probucol’s antioxidant properties. However, in view of the recent finding that probucol results in lowered HDL2b levels in hypercholesterolemics27, probucol use in atherosclerosis must be viewed with caution.

Our results highlight the potential of antioxidants in preventing, and possibly reversing, the natural course of carotid atherosclerosis.

Finally, two recent meta-analyses of randomised, controlled trials28,29 found that lowering serum cholesterol through modified diets or medications did not reduce stroke mortality or morbidity in middle-aged men. These results were further substantiated by an even more recent Swedish report30 which showed no difference in carotid-intimal-media thickness or plaque status in a group with comprehensive risk reduction (including a 9% LDL cholesterol decrease) after 3.5 years of observation.

Acknowledgment. The KL Jordan Research Group gratefully acknowledges the support in these studies of PORIM (Kuala Lumpur, Malaysia). Additionally, we wish to thank Dr Hemmige Bhagavan for his review of the manuscript and subsequent useful suggestions.


  1. Salonen JT, Yla-Herttuala S, Yamamoto R, Butler S, Korpella H, Salonen R, Nyyssonen K, Palinski W, Witztum JL. Autoantibody against oxidized LDL and progression of carotid atherosclerosis. Lancet 1992; 339: 883-887.
  2. Witztum JL and Steinberg D. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest. 1991; 88: 1785-1792.
  3. Steinberg D and Workshop Participants. Antioxidants in the prevention of atherosclerosis. Circulation. 1992; 85: 2338-2344.
  4. Esterbauer H, Dieber-Rotheneder M, Striegel G, Waeg G. Role of vitamin E in preventing the oxidation of low-density lipoprotein. Am J Clin Nutr. 1991; 3: 314S-321S.
  5. Carew TE, Schwenke DC, Steinberg D. Antiatherogenic effect of probucol unrelated to its hypocholesterolemic effect: evidence that antioxidants in vivo can selectively inhibit low density lipoprotein degradation in macrophage-rich fatty streaks slowing the progression of atherosclerosis in the WHHL rabbit. Natl Acad Sci. 1987; 84: 7725-7729.
  6. Mao SJT, Yates MT, Parker RA, Chi E. M, Jackson RL. Attenuation of atherosclerosis in a modified strain of hypercholesterolemic Watanabe rabbit with use of a probucol analogue (MD29, 311) that does not lower serum cholesterol. Art and Thromb. 1991; 11: 1266-1275.
  7. Rimm EB, Stampfer MJ, Ascherio A, Giovanucci E, Colditz GA, Willett WC. Vitamin E consumption and the risk of coronary heart disease in men. N Eng J Med. 1993; 328: 1450-1456.
  8. Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vit. E and risk of coronary disease in women. N Eng J Med.1993; 328: 1444-49.
  9. Gey KF. Ten-year retrospective on the antioxidant hypothesis of arteriosclerosis. J Nutr Biochem. 1995; 6: 206-236.
  10. Bonner LL, Kanter DS, and Manson JE. Primary Prevention of Stroke. New Engl J Med 1995; 333: 1392-1400.
  11. Stephens NG, Parsons A, Schufield PM, Kelly F, Cheeseman K, Mitchinson NJ, Brown MJ. Randomized controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347:781-6.
  12. Kritchevsky SB, Shimakawa T, Dennis B, Eckfeldt J, Carpenter M, Heiss G. Dietary antioxidants and carotid artery wall thickness: ARIC study. Circulation 1995; 92: 2142-2150.
  13. Delong DM, Delong R, Wood PD, Lippel K, Rifkind BM. A comparison of methods for the estimation of plasma low- and very low-density lipoprotein cholesterol. J Am Med Assoc. 1986; 256: 2372-2377.
  14. Ohishi N, Ohkawa H, Miike A, Tatano T, Yagi K. A new assay method for lipid peroxides using a methylene blue derivative. Biochem Intl. 1985; 10: 205-211.
  15. Mihara M, Uchiyama M, Fukuzawa K. Thiobarbituric acid value on fresh homogenate of rat as a parameter of lipid peroxidation in aging; CCl4 intoxication and vitamin E deficiency. Biochem Med. 1980; 23: 302-311.
  16. Bieri JG, Tolliver TJ, Catigniani CL. Simultaneous determination of -tocopherol and retinol in plasma and red cells by high pressure liquid chromatography. Am J Clin Nutr. 1979; 32: 2143-2149.
  17. Galvez A, Badimon L, Badimon J, Fuster V. Electrical aggregometry in whole blood from human, pig, and rabbit. Thromb and Hem. 1986; 56: 128-132.
  18. Salonen JT, Nyssonen K, Parviainen M, Kantola M, Kantola M, Korpela H, Solonen R. Low plasma b-carotene, vitamin E and selenium levels associated with accelerated carotid atherogenesis in hypercholesterolemic Finnish men. Circulation 1993; 87: 2, abstract.
  19. Bierenbaum ML, Reichstein RP, Bhagavan HN, Watkins TR Relationship between serum lipid peroxidation products in hypercholesterolemic subjects and vitamin E status. Biochem. Int. 1992; 28: 57-66.
  20. Qureshi AA, Qureshi N, Hasler-Rapacz JO, Weber FE, Chaudhary V, Crenshaw TD, Gapor A, Ong ASH, Chong YH, Peterson D, Rapacz J. Dietary tocotrienols reduce concentrations of plasma cholesterol, apolipoprotein B, thromboxane B2 and platelet factor 4 in pigs with inherited hyperlipidemias. Am J Clin Nutr. 1991; 53: 1042S-1049S.
  21. Qureshi AA, Qureshi N, Wright JJK, Shen Z, Kramer G, Gapor A, Chong YH, Dewitt G, Ong ASH, Peterson DM, Bradlow BA. Lowering of serum cholesterol in hypercholesterolemic humans by palmvitee. Am J Clin Nutr 1991; 53: 1021S-26S.
  22. Wahlqvist ML, Krivokuca-Bogetic Z, Lo CS, Hage B, Smith R, Lukito W. Differential serum responses of tocopherols and tocotrienols during vitamin supplementation in hypercholesterolemic individuals without change in coronary risk factors. Nutr Res. 1992; 12: Suppl. 1, S181-S201.
  23. Watkins TR, Lenz P, Gapor A, Struck M, Tomeo A, Bierenbaum ML. g-tocotrienol as a hypocholesterolemic and antioxidant agent in rats fed atherogenic diets. Lipids 1993; 28: 1113-1118.
  24. Bierenbaum ML, Fleischman AI, Raichelson RI, Hayton T, Watson PB. Ten-year experience of modified-fat diets on younger men with coronary heart disease. Lancet 1973; 2: 1404-1407.
  25. Miettinen TA, Huttunen JK, Naukkaunien V, Strandberg T, and Watson PB. Long-term use of probucol in the multifactorial primary prevention of vascular disease. Am J Card. 1986; 57: 49H-54H.
  26. Bocan TMA, Mazur MJ, Mueller SB, Charlton G, Kieft KA, Krause BR. Atherosclerotic lesion development in hypercholesterolemic Japanese quail following probucol treatment: a biochemical and morphological evaluation. Pharmacol. Res. 1994; 29: 65-76.
  27. Johansson J, Olsson A, Bergstrand L, Elinder LS, Nilsson Sven, Erikson U, Molgaard J, Holme I, Waldius G. Lowering of HDL2b by probucol partly explains the failure of the drugs to affect femoral atherosclerosis in subjects with hypercholesterolemia. Arterio. Vasc. Biol. 1995; 15: 1049-1056.
  28. Atkins D, Psaty BM, Koepsell TD, Longstreth WT, Larson EB. Cholesterol reduction and the risk of stroke in men. A meta-analysis of randomized, controlled trials. Ann. Intern. Med. 1993; 119: 136-145.
  29. Herbert PR, Gaziano JM, Hennekens CH. An overview of trials of cholesterol lowering and risk of stroke. Arch. Int. Med. 1995; 155: 50-55.
  30. Suurbüla M, Agewall S, Fagerberg B, Wendehag I, Wikstrand J on behalf of the Risk Intervention Study (RIS) Group. Multiple risk intervention in high-risk hypertensive patients. Arterioscl. Thromb. Vasc. Biol. 1996; 16: 462-170.

Antioxidant effects of tocotrienols in patients with hyperlipidaemia and carotid stenosis-2 year experience
DK Kooyenga, M Geller, TR Watkins, A Gapor, E Diakoumakis, ML Bierenbaum
Asia Pacific Journal of Clinical Nutrition (1997) Volume 6, Number 1: 72-75

Copyright © 1993 [Asia Pacific Journal of Clinical Nutrition]. All rights reserved.

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