It seems that palm tocotrienol has multi-targeted mechanistic approach that could be useful for stroke therapeutics and prevention. Once a person is diagnosed with a mini stroke, one has extremely high risk for another big stroke. These people are at high risk factors for stroke that would be subjected to secondary prevention. Under these conditions, palm tocotrienols may have promise by preventing clot formation, neuroprotection, and rescue through arteriogenesis.
Aspirin is known to have certain complications including gastrointestinal tract bleedings. In the case of tocotrienol, Dr. Chandan Sen mentioned that they have been studying over hundreds of patients for the past seven years through IRB (Institutional Review Board) approved studies, and have received no adverse effects reported so far. The on-going clinical trials on victims of mini-stroke did not report any adverse effects as well. Tocotrienol has already received GRAS (Generally Recognized as Safe) (GRN Notice No 307), status by USFDA.
If somebody is taking aspirin for quite some time and stop taking aspirin for the next 48 hours, the anti-clotting properties will start to lose because about one tenth of the platelets in the body is made new every day. If one does not have aspirin memory in the new platelets fragments that had just produced, anti-clotting properties will not retain. A study has shown that dietary intake of tocotrienols for a few months will load into subcutaneous fat tissues and that fat tissues releases tocotrienol gradually into the bloodstream, signifying a time-release system for tocotrienol. Additionally, it is also observed that even 10 days without tocotrienol supplementation, one still has a complete arachidonic acid induced platelets aggregation.
Below are some of the relevant references:
Blood clot formation prevention
Effect of tocotrienol derivatives on collagen and ADP-induced human platelet aggregation. Mahadevappa, V.D., et.al (1991). International Palm Oil Conference-Nutrition and Health Aspect of Palm Oil.
Arteriogenesis
Neuroprotection
- Sen C.K., et.al (2000). Molecular basis of vitamin E action. Tocotrienol potently inhibits glutamate-induced pp60(c-Src) kinase activation and death of HT4 neuronal cells. J Biol Chem.
- Khanna, S., et.al (2003). Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration. J Biol Chem.
- Khanna, S., et.al (2010). Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. J Neurochem.
- Khanna S., et.al (2013). Loss of miR-29b following acute ischemic stroke contributes to neural cell death and infarct size. J Cereb Blood Flow Metab.
- Rink, C. et.al (2011). Tocotrienol vitamin E protects against preclinical canine ischemic stroke by inducing arteriogenesis. J Cereb Blood Flow Metab.