*Dietary Reference Intake not established.
Other ingredients: olive oil, rosemary oil, ascorbyl palmitate. May contain beeswax. Softgel: gelatin, carob.
AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, eggs, fish, or shellfish.
Suggested Use
Take one to four softgels daily with a fat-containing meal, or as directed by a qualified health care practitioner. If you are concerned about maintaining healthy blood lipid balance, combine with a diet low in saturated fats.
Main Applications
As reported by literature:
• Antioxidant.
• Cardiovascular disease.
• Anticarcinogens.
• Healthy blood lipids.
Source
Palm.
Pregnancy / Nursing
No studies have been conducted. Best to avoid.
Cautions
• Possible interaction with Warfarin (Coumadin). Vitamin E complex may "thin" the blood. Consult with a physician if you are using anticoagulants or if you have clotting problems.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Tocotrienols
Vitamin E was discovered at the University of California at Berkeley in 1922. Its early isolation from plant oils, notably corn, soybean, and olive oils, identified four compounds: alpha-, beta-, gamma-, and delta- tocopherols. Recently, four corresponding structural analogs of tocopherols have been discovered in barley, palm, and rice bran oils.These are termed alpha, beta, gamma, and delta tocotrienols. Tocotrienols are structurally different, having three unsaturated positions in the phytyl "tail" of the molecule. Tocotrienols represent the vanguard of novel, multi-action products with highly promising potential to safeguard health and function. |
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Physiological properties of tocotrienols:
Antioxidant Studies by Dr. Lester Packer and his group at Berkley showed that tocotrienols possess 40 to 60 times higher activity than tocopherols against iron-catalyzed lipid peroxidation of cellular membranes. In addition, the alpha isomer possessed 6.5 times better protection of the cytochrome P-450enzyme complex against oxidation. Tocotrienols' higher antioxidant properties are due to the following:
(1.) More efficient and uniform penetration of membrane bilayers.
(2.) Higher recycling efficiency.
(3.) Stronger disordering of membrane lipids, causing more efficient interaction with lipid radicals.
Cardiovascular disease
Atherosclerosis leading to coronary heart disease and stroke is the leading cause of death for those enjoying the western lifestyle. An inverse relationship exists between the development of atherosclerosis and serum concentration of tocotrienols. In a study with 27 hypercholesterolemic patients with serum cholesterol levels of 240-310mg/mL, administration of 200mg of palm tocotrienols for 4 weeks caused statistically significant drops of 15-22% in total cholesterol and 10-20% in LDL. Seven non-responders (all with cholesterol >300mg/dL) were given additional 100mg TRF, which caused a dramatic drop of 35-40% total serum cholesterol. More excitingly, a double-blind trial by Tomeo et al showed that 28% of subjects with carotid stenosis administered tocotrienols showed regression of arterial blockage, while all of those in the placebo group either had no improvement or actually showed increases in stenosis over the same time frame.
The mechanism of action for the hypolipidemic effects has yet to be elucidated, but suppression of HMG-CoA reductase at the post-transcriptional level is believed to be involved. Unlike the mechanism of "statin" drugs (blocking of the HMG CoA reductase receptor sites), TRF seems to act by increasing the degradation of HMG CoA reductase enzyme, and is therefore devoid of the statin drugs' side-effects (notably carcinogenicity, myopathy, and depletion of CoQ10 levels, particularly in the heart tissue).
The prevention of the oxidation of LDL is also a likely reason for tocotrienols' cardiovascular benefits. Oxidation of LDL (low-density lipoproteins) and VLDL (very low density lipoproteins) is now known to be a key initiating event in the initiation of atherosclerosis. Reduced oxidized lipids including LDL and arterial damage were noted. Another key factor in the cardiovascular mortality is the formation of blood clots, which can become trapped in blood vessels narrowed by atherosclerotic plaques. Animals fed tocotrienols show a potent reduction of the production of clotting factors such as thromboxane B2 and platelet factor IV, and a resulting decrease of 20-26% in platelet aggregation.
Anticarcinogens
Tocotrienols exert a protective effect via free radical scavenging, since free radicals can induce DNA damage and carcinogenesis. Supplementation of tocotrienols in rats induced with the potent liver cancer agents DMBA (Dimethyl-benz-anthracene) and aflatoxin demonstrated that tocotrienols delayed the impact of cancer agents. Similar effects were observed with mammary tumors.
Yu and colleagues reported that all tocotrienols, and delta tocopherol -- but not alpha or other tocopherols -- could induce apoptosis (cellular suicide) in human breast cancers in vitro.
Angiogenesis, the fancy name for the creation of new blood vessels, is an important aspect of cancer development since tumors require new blood vessels to provide them with nutrients in order to grow and spread. Angiogenesis is also involved in rheumatoid arthritis, psoriasis and diabetic retinal disease. Tocotrienols seem to be able to block this potentially dangerous process. One study found that tocotrienols can block angiogenesis in bovine and human cells. A further study involving mouse and chick embryo models found that the use of tocotrienols as a dietary supplement clearly suppresses new blood vessel formation without damaging the preexisting vessels. The process of angiogenesis requires cellular signals to be sent to endothelial cells which respond by proliferating, migrating and rolling into tubes to begin blood vessel formation. One such signal is the fibroblast growth factor (FGF). Tocotrienols appear to block the signaling pathway that occurs when FGF binds to its receptor on cell surfaces, thereby stopping the cells from beginning angiogenesis.
Tocotrienols also help prevent DNA damage. A randomized, double-blind, placebo-controlled study found that measurements of DNA damage were decreased after tocotrienol supplementation for three months compared to initial levels and they stayed low after 6 months. This decrease was especially pronounced in older adults, who also tend to have the highest initial levels of DNA damage. A fairly serious form of DNA damage is when both strands of a DNA molecule are broken. Reparation of such a break is performed by a method known as homologous recombination repair, where sister chromatids (identical packages of DNA) cross over and exchange genetic information to make sure that none is lost. This sister chromatid exchange (SCE) is a spontaneous reaction to DNA damage during DNA replication and appears to increase in response to ROS. Although it is normally accurate, errors in the repair can lead to DNA alteration, which in turn contributes to carcinogenesis. Older participants of the study had decreased counts of SCE after 6 months of tocotrienol supplementation, indicating that their DNA had become more stable. They also showed a decreased amount of urinary 8-OHdG after 6 months of supplementation, which is a marker of oxidative stress. Tocotrienols' protective effect is likely due to its antioxidant characteristics which can prevent DNA from being damaged.
Advantages of Palm vs. Rice as a Tocotrienol Source
1. Naturally, palm has a higher concentration of tocotrienols than rice.
2. Delta tocotrienol is the most potent natural HMG-CoA reductase inhibitor. Rice is devoid of this isomer.
3. High alpha-tocopherol attenuates gamma tocotrienol. Qureshi (1996) has shown that preparations containing high alpha tocopherol (above 30% ratio) would attenuate the activity of gamma tocotrienol. Palm has a ratio of 20-21% compared with over 40% for rice.
4. Palm has a higher concentration of other phytonutrients including Squalene, Co-Enzyme Q10, phytosterols, and alpha- and beta-carotene.
5. Palm is high in mono- and polyunsaturated fatty acids.
6. The presence of monoglycerides and diglycerides in TRF acts as an emulsifying agent, thereby increasing solubilization and hence bioavailability.
7. Most of the research (>90%) has been conducted on palm-derived tocotrienols.
References
i. Serbinova E, Kagan V, Han D, Packer L. (1991), "Free radical recycling and intramembrane mobility in the antioxidant properties of alpha-tocopherol and alpha-tocotrienol." Free Radic Biol Med 10(5): 263-75.
ii. Tomeo AC, Geller M, Watkins TR, Gapor A, Bierenbaum ML. (1995), "Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotid stenosis." Lipids 1995 Dec; 30(12): 1179-83.
iii. Quershi AA, et al., (1996). "Dietary Alpha-Tocopherol Attenuates the Impact of Gamma-Tocotrienol on hepatic 3-Hydroxy-3-Methylglutaryl Co enzyme A". J. Nutr; 126: 389-394.
iv. Yu W, Simmons-Menchaca M, Gapor A, Sanders BG, Kline K. (1999), " Induction of apoptosis in human breast cancer cells by tocopherols and tocotrienols." Nutr Cancer. 1999; 33(1): 26-32.
v. Goh SH, Hew NF, Norhanom AW, Yadav M. (1994), "Inhibition of tumor production by various palm oil tocotrienols." Int J Cancer 15: 529-31.
vi. Kamat SP, et al., (1995). "Tocotrienols from Palm Oil as potent inhibitors of lipid peroxidation and protein oxidations in rat brain mitochondria". Neurosci Left195: 179-82.
vii. Das S, et al. (2008) Cardioprotection with palm oil tocotrienols: comparision of different isomers. Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H970-8.
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