It should be noted that of all the forms of tocotrienol, the delta and gamma forms are the most potent. This is simply because the molecular structure of the ‘head’ region of the vitamin for those two forms leaves the molecule less restricted. It is able to work better as an antioxidant.
The cholesterol lowering effects of tocotrienols was first studied in 1991 by the University of Wisconsin. At first, patients received a mix of tocotrienols and tocopherols. This saw a drop in total cholesterol of 15-22% and a drop in LDL cholesterol (bad cholesterol) 10-22%. The results were slightly disappointing, however, when it was shown that 15% of patients did not show any improvement in their cholesterol levels. Trials on these patients thus continued with purely delta- and gamma-tocotrienols. After four weeks, cholesterol for these patients dropped 35-40%!
Tocotrienols are a good option for lowering cholesterol levels compared to the more standard cholesterol lowering option: statins. Statin drugs are used to inhibit LDL cholesterol, but are also associated with side effects, such as muscle pain and fatigue. This all has to deal with the mechanism in which Statin acts to lower cholesterol. Cholesterol synthesis occurs in a pathway (a series of chemical reactions that act in a step-wise fashion) starting from the initial enzyme which ends in the eventual creation of cholesterol. Statins are called competitive inhibitors of cholesterol synthesis. This means they works directly on the HMG CoA reductase enzyme (the protein responsible for initiating the cholesterol synthesis pathway) by competing directly with the normal substrate (the molecule on which the enzyme acts) for HMG CoA reductase. In this regard, statins are incredibly effective in reducing cholesterol levels by shutting down the pathway, but they unfortunately also reduce the production of some essential proteins in the process.
Tocotrienol is considered a ‘non-competitive’ inhibitor of HMG coA reductase. This is because it does not compete directly with HMG coA reudctase’s substrate in the same way that statin does. It actually works further down the synthesis pathway to down-regulate cholesterol synthesis. The tail of the tocotrienol molecule releases an intermediary molecule of the pathway. Your body recognizes this increase of that molecule so the pathway regulates itself by decreasing the reaction of HMG coA reductase (so as to not overproduce on that molecule). Tocotrienol has also been shown to degrade HMG coA reductase as well. Consequently, this reduces the production of cholesterol (since HMG coA reductase does not react) but does not reduce CoQ10 production (since the entire pathway isn’t shut down and the intermediary steps that lead to CoQ10 production are not hindered).