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Can Vitamin E Really Help Cholesterol?
While researchers consistently demonstrate that vitamin E can lower cholesterol levels in animal and in vitro studies, the results of human studies have been mixed. This article discusses the key reasons for this difference and the limitations of tocopherols in the treatment of hypercholesterolemia. You will also learn how research into a new group of vitamin E vitamers is providing new insights into the antioxidant and cholesterol-lowering benefits of this vitamin.
by Brad Chase
Vitamin E refers to a group of eight related, fat-soluble vitamers. Four of these are tocopherols while the other four vitamers are tocotrienols.
The most common form of vitamin E used in studies are the tocopherols especially alpha-tocopherol.
In addition, alpha-tocopherol is commonly regarded as the most active form of vitamin E although gamma-tocopherol is the most common form of the vitamin found in the American diet.
Excellent dietary sources of vitamin E include the oils of safflower, sunflower, wheat germ, palm, corn and soybean as well as nuts, whole grain, avocado, asparagus, pumpkin, spinach and green, leafy vegetables.
Because vitamin E can be obtained from various dietary sources, its deficiency is rare except in people who cannot absorb or metabolize dietary fat (vitamin E is fat-soluble and, therefore, needs fat to be absorbed).
While the body needs vitamin E for a number of important biological processes, new evidence from recent studies indicates that vitamin E supplementation may not provide clear health benefits.
However, there are indications that the alpha-tocopherol commonly found in vitamin E supplements may not be the most bioactive form of the vitamin. In fact, current research into the different forms of vitamin E shows that tocotrienols are more active than tocopherols even though a mere 1% of vitamin E research involved them.
These new studies show that tocotrienols
A 2005 report from the National Academy of Sciences showed that Americans are only consuming half of the recommended daily allowance (RDA) of vitamin E. This is mostly because we are consuming more processed foods.
Some experts believe that this vitamin E shortfall contributes to the rising incidence of hypercholesterolemia and cardiovascular diseases.
However, the cholesterol-lowering effect of vitamin E is still hotly debated. While some studies found that vitamin E supplementation can reduce cholesterol levels, others found no such link. In vitro and animal studies repeatedly demonstrate that vitamin E can lower cholesterol levels and also reduce the risk of atherosclerosis but the results of human studies are mixed.
Researchers have given different reasons for the lack of universal evidence for the cholesterol-lowering effect of vitamin E in human studies.
Two of those arguments are especially noteworthy because they shed more light on how vitamin E can deliver good results in the treatment of hypercholesterolemia.
After more than 50 years of concentrating vitamin E research on tocopherols, researchers are finally studying tocotrienols and with good results too.
The major difference between tocotrienols and tocopherols is the presence of 3 double bonds in their side chains. Tocopherols have 3 single bonds at those positions.
In one study, researchers showed that tocotrienols are involved in the production of cholesterol in the liver. Specifically, they inhibit the enzyme, HMG-CoA reductase. Therefore, they can reduce blood cholesterol levels in the same way as the statins found in popular prescription cholesterol drugs.
HMG-CoA reductase is involved in the mevalonate pathway used to synthesize sterols in the liver.
Because cholesterol is synthesized in the same pathway, blocking this enzyme reduces the production and blood level of cholesterol.
Another study done by a team of researchers from Universiti Sains Malaysia investigated the effect of mixed tocotrienols on cholesterol levels. This study was published in the journal, Functional Foods in Health and Disease in 2011.
The researchers divided 32 patients with high blood cholesterol into 2 groups and gave one group 300 mg/day of mixed vitamers of vitamin E while the placebo group received 300 mg/day of soya bean oil for 6 months.
The vitamin E mixture given to these volunteers contained 75% alpha, delta and gamma tocotrienols obtained from palm oil and 25% tocopherols. The combination was formulated in a special self-emulsifying delivery mechanism to improve the absorption of the vitamers.
The soya bean oil given to the placebo group is known for its high tocopherol content.
After 4 months of supplementation, total cholesterol decreased by 8.9% and LDL (low-density lipoprotein or “bad”) cholesterol decreased by 12.8% in the mixed tocotrienols group compared to the soya bean group. These reduction in cholesterol levels continued to the end of the study. By then LDL cholesterol level had fallen by 17.4% while total cholesterol was lowered by 10.8%.
The results of the study showed that tocotrienols did not affect the levels of HDL (high-density lipoprotein or “good”) cholesterol and triglycerides.
With such promising results, the Malaysian government sponsored two clinical trials to further investigate the effect of tocotrienols on platelet functions and cholesterol levels in order to determine the benefits of this group of vitamin E vitamers in the treatment of cardiovascular diseases.
Besides simply lowering cholesterol levels, another important mechanism by which vitamin E reduces the risks of atherosclerosis and other cardiovascular disorders is by inhibiting the oxidation of cholesterol especially LDL cholesterol.
Although LDL cholesterol is often called “bad” cholesterol, low-density lipoprotein is simply a carrier for cholesterol. While LDL is responsible for transporting cholesterol through the blood, HDL removes cholesterol from the blood.
When reactive oxygen species and free radicals oxidize LDL cholesterol, they turn it “bad” and the oxidized lipoprotein thickens the arteries by adhering to their walls.
By preventing the oxidation of LDL cholesterol, it is possible to prevent atherosclerosis even when the blood level of LDL cholesterol is high. This also means that without the protection of antioxidants, people with low LDL cholesterol are also not well protected.
Therefore, scientists believe that the antioxidant property of vitamin E can inhibit lipid peroxidation and prevent atherosclerosis.
However, the results of human studies have not consistently supported this theory.
There are two main reasons for the difference between the expected and actual performance of vitamin E as an antioxidant. The first reason involves the type of oxidation reaction vitamin E inhibits and the second reason is the timing of vitamin E supplementation.
The antioxidant effect of vitamin E only blocks oxidation by free radicals. This is the reason it is ineffective against cholesterol oxidation caused by the other 3 types of oxidation.
Secondly, the oxidation of LDL cholesterol in humans occurs over a long period of time. However, in studies, cholesterol oxidation is triggered just before it is countered by vitamin E. Therefore, in animal and in vitro studies, vitamin E can effectively inhibit a new and ongoing oxidation.
However, in humans, the damage caused by cholesterol oxidation would have set in for a long while.
This means that it would take years of vitamin E supplementation before the first signs of antioxidant protection are seen. Since human studies never take that long, it is expected that no effect on cholesterol oxidation would be reported in such studies.
Therefore, vitamin E supplementation must be started early on for it to be effective and reduce the risk of atherosclerosis.
A study published in the journal, Circulation, in 2000 investigated the exact mechanism by which vitamin E reduces the risk of atherosclerosis by inhibiting the oxidation of LDL cholesterol.
The researchers used cultured human aortic muscle cells in this in vitro study. They showed that a specific type of receptor known as CD36 scavenger receptor was found on the muscle cells of the aorta. This receptor is required for oxidized LDL to exert its damage to the muscle cells of the heart.
On exposing these muscle cells to alpha-tocopherol, the researchers noted that the number of CD36 scavenger receptors fell and the uptake of oxidized LDL was reduced.
The study showed that vitamin E protects the heart and blood vessels from the damage caused by oxidized LDL cholesterol by downregulating the receptor needed for the uptake of this type of cholesterol.
Therefore, vitamin E can reduce the levels of LDL cholesterol, reduce the oxidation of LDL cholesterol and block the actions of oxidized LDL cholesterol.
A 2003 study published in the journal, BioFactors, provided a different but related insight into how the antioxidant property of vitamin E reduces the risk of atherosclerosis.
This study showed that vitamin E inhibits the growth of the smooth muscles of the heart and blood vessels by reducing the activity of a protein known as kinase C. The growth of these smooth muscles can block blood vessels, restrict blood flow and cause ischemic heart disease.
The study also identified that vitamin E can prevent homocysteine, a toxic metabolite of amino acid syntheses, from inducing the overgrowth of these smooth muscles.
A 1996 study published in the journal, Lancet, identified the benefits of long-term vitamin E supplementation.
In that study, the researchers recruited over 2,000 patients suffering from atherosclerosis. They then divided these volunteers into 2 groups: the placebo group and treatment group. The treatment group received 800 IU/day of alpha-tocopherol capsules for as long as needed (the average length of vitamin E supplementation was 510 days).
The study results showed that vitamin E supplementation reduced the rate of myocardial infarction in patients with atherosclerosis.
Just as importantly, the researchers discovered that the benefits of vitamin E was seen only after 1 year of continual supplementation.
A 2008 study published in the American Journal of Physiology: Heart and Circulatory Physiology compared the potencies of the 3 forms of tocotrienols in improving cardiovascular health.
The researchers fed different groups of rats with alpha, gamma and delta tocotrienols as well as tocotrienol-rich extract of palm oil. The results of the study showed that all 4 forms of treatment reduced the damaged caused myocardial infarction and heart ischemia.
By comparing the results obtained from the 3 forms of tocotrienols to the results obtained from the mixed tocotrienol fraction of palm oil, the researchers determined that the most potent (with regards to cardioprotection) of the tocotrienols was the gamma form followed by the alpha and then the delta forms.
In addition, the researchers also noted that the cardioprotective properties of tocotrienols involved the stabilization of a protein complex in cells known as proteasome.
A 2007 study published in the journal, Vitamins and Hormones, reviewed the state of tocotrienol research. The authors of the paper recognized the state of current research on tocotrienols compared to tocopherols and identified that previous studies found that tocotrienols can lower cholesterol levels and also have anticancer properties.
Both the cholesterol-lowering and antioxidant properties of tocotrienols were shown to be useful for reducing the risks of heart diseases such as atherosclerosis, ischemia and arrhythmias.
Lastly, the study identified another little-known benefit of tocotrienols. Tocotrienols have been proven to precondition the heart and blood vessels for other drugs and supplements that improve cardiovascular health.
Therefore, tocotrienol supplementation was recommended as a therapeutic preconditioning agent.
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Resterol is a natural cholesterol remedy that helps lower bad cholesterol (LDL) and raise good cholesterol (HDL). Works best when used in conjuction with a healthy diet such as the Paleo Diet.