Next, intracellular protein com- plexes called inflammasomes are activated. Inflammasomes trigger the maturation of the highly inflammatory IL-1β & IL-18. When inflammasomes, which are also sensors and reg- ulators of the colonic microbio- ta are activated, the gut micro- biota is also altered. Could this altered composition influence events in the liver? I believe so. Changes in the composition of the microbiota as a result of inflammasome activation or
dysbiosis trigger the cytokine cascade
with initiation
progression of inflammatory liver disease.
A cautiously optimistic idea is now taking hold that invokes using mitochondrial and bac- terial induced symbiosis of the gut microbiota to track, target and treat a plethora of diseases, even ones beyond the confines of the gastrointestinal tract. Adding tocotrienols to this dual approach creates a therapeutic trinity of natural, safe agents.
References: and
Bird L. Innate immunity: Linking mitochon- dria and microbes to inflammasomes. Nat Rev Immunol. 2012 Mar 9;12(4):229
Kubes P, Mehal WZ. Sterile inflammation in the liver. Gastroenterology. 2012 Nov;143(5):1158-72.
Day CP, James OF. Steatohepatitis: a tale of two “hits”? Gastroenterology. 1998 Apr;114(4):842-5
Sanyal AJ, et al. Nonalcoholic steatohepatitis: association of insulin resistance and mito- chondrial abnormalities. Gastroenterology120, 1183–1192 (2001)
Henao-Mejia J, et al. Inflammasome-mediat- ed dysbiosis regulates progression of NAFLD and obesity. Nature482, 179–185 (2012)
Korecka A, Arulampalam V. The gut micro- biome: scourge, sentinel or spectator? J Oral Microbiol. 2012;4. doi: 10.3402/jom.v4i0.9367. Epub 2012 Feb 21.
Why Can’t They Just Get Along? The Truth about Alpha-Tocopherol and Its Vitamin E Cousins
Is alpha-tocopherol a kind of molecular bully, gifted with its own special passenger train (its own transport protein), by which it can reach any tissue in the body better and faster than other Vitamin E fractions? Does it actually inhibit the absorption of other forms of Vitamin E? Is it possibly dangerous?
The answers are nuanced, as biology always is. All forms of Vitamin E have their own mo- lecular gifts, and certainly al- pha-tocopherol is a potent an- tioxidant, a “fertility factor” necessary for reproduction, and necessary for many bodily func- tions and yes, it does have its own transport protein.
18 Focus April 2013
On the other hand, it’s only one of eight. Alpha-tocopherol has been erroneously conflated with “Vitamin E” in study after study, as if it alone represented the entire family of molecules. Yet large scale investigations into al- pha-tocopherol’s benefits when given alone have been contradic- tory at best. One of the biggest studies—spanning 174 centers and over 7000 individuals, called the Heart Outcomes Prevention Evaluation (HOPE) trial, and the subsequent HOPE TOO tri- al—found that in patients with vascular disease or diabetes mellitus, long-term alpha-to- copherol supplementation did not prevent cancer or major car-
diovascular events.1 Even more
concerning, a 2010 meta-analysis of 22 studies on alpha-tocoph- erol and stroke, from Harvard’s Brigham and Women’s Hospi- tal found that alpha-tocopherol supplementation “increased the risk for hemorrhagic stroke by 22% and reduced the risk of isch- emic stroke by
10%...Given the relatively small risk reduction of ischemic stroke and the general- ly more severe outcome of hem- orrhagic stroke, indiscriminate widespread use of vitamin E should be cautioned against.”2,3 In addition, high doses of al- pha-tocopherol (over 400 mg/ day) may prevent absorption of the other Vitamin E fractions and
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