Why Vitamin E Is Crucial (Fish Oils Reduce Vitamin E)

Vitamin E is classified under 8 different names, 4 tocopherol and 4 tocotrienols, both the tocopherol and tocotrienol have α β γ δ designations. The difference between tocopherol and tocotrienol is the saturated side chain of the natural (tocopherol) version. All tocopherol and tocotrienol are absorbed and incorporated in similar ways, by way of passive diffusion and being transported by micelles. Due to the fragile nature of fish oils vitamin E can be reduced. In fact, fish oils are one of the main ways to reduce vitamin E. The breakdown of fish oils generates reactive oxygen species (ROS). These ROS need to be stopped, one way of stopping the ROS is vitamin E. See the description below.

What Does Vitamin E Do?

The absorption rate of oral alpha-tocopherol is significantly higher than gamma, delta, and the tocotrienols. Tocotrienols, compared to alpha-tocopherol do not appear to sustain themselves in blood plasma levels, even when tocotrienols intake is higher. This seems to be caused by the transport from the liver in the form of tocopherol transfer protein (α-TTP) a mechanism that determines the vitamin E plasma levels and has a strong affinity for alpha-tocopherol[5]. The tocotrienols have a habit of disappearing shortly after oral intake, compared to alpha-tocopherol[6]. Because Vitamin E is fat-soluble, other forms of Vitamin E (tocotrienol) could be transported by TRP and HDL. Although studies show that little tocotrienols are incorporated into blood plasma(alpha-tocopherol is more liked), this can be changed by a self-emulsifying preparation (but even without preparation tocotrienol is transported to the tissues). Studies with mice showed that oral supplementation with tocotrienol, without the α-TTP organs were fully saturated, however after supplementation stopped, the accumulated tocotrienol levels disappeared within 2 months.

Animal studies

Controlled animal trials with diabetic rats show that tocotrienols-rich fractions from palm improve blood glucose, dyslipidemia, and oxidative stress. Tocotrienols-rich fractions supplemented rats fare better than alpha-tocopherol supplemented rats in endurance (equal amount of the supplement). Oral administration of TRF outperformed alpha-tocopherol in DBTC-induced (chronic pancreatitis) rats by alleviating pancreatic inflammation and fibrosis. In rabbits, tocotrienol-rich fragments reduced experimental atherosclerosis by way of anti-oxidant activity. Oral supplementation in dogs shows that tocotrienol is raised after 2 hours and maximized after 12 hours in blood levels (similar to a-tocopherol) and suggests antioxidant potential[16]. Interesting, tocotrienol-rich extract seem to work better than the pure form tocotrienol and alpha-tocopherol gamma-tocopherol was superior versus alpha-tocopherol in decreasing platelet aggregation and delay intra-arterial thrombus formation.

Human cells

Testing in animals with human cells shared many of the positive attributes shown in animal studies. Human colon cancer cells implanted in baby mice showed a potent anticancer effect of TRF and is associated with the regulation of Wnt signal pathways, this pathway “regulates crucial aspects of cell fate determination, cell migration, cell polarity neural patterning, and organogenesis during embryonic development”. Alpha-tocopherol showed no improvement in the growth of human breast cancer cells, while tocotrienol inhibited 50% of the cell line[21]. Both Tocopherols and tocotrienols offer protection of cerebellar granule cells against methylmercury. Γ Tocopherol and its hydrophilic metabolite show to have inhibiting effects of COX-2 activity in intact human cells (more effective than α tocopherol). Tocotrienols have been shown to inhibit certain tumor angiogenesis.

Vitamin E in clinical trails

Because of the lack of interest in the other vitamin E vitamers alpha-tocopherol, the human (clinical) trials are sparse. The studies with humans show that there is activity to show the activity of the vitamin E vitamers besides (alpha-tocopherol) in humans.

  • Malaysian women had 65% more concentrated forms of tocotrienol (α-T3, γ-T3 and δ-T3) in the adipose tissue of the benign lumps in comparison to the women with malignant breast lumps.
  • Tocotrienol has been shown to be useful by type 2 diabetics in the prevention and treatment of hyperlipidemia and atherogenesis.
  • Palmvitee (contains more than 200% tocotrienols than tocopherol), has a hypocholesterolemic effect.
  • An improvement towards in arterial compliance was seen after 2 months of SF-TRE (self-emulsifying preparation of tocotrienol rich vitamin E), although no SF-TRE on serum lipids was seen.

Different functions between alpha-tocopherol and the other vitamers

The different molecular structure in the different vitamers has different properties. Studies show that tocotrienol properties are different in a number of ways. Tocotrienols has been shown to activate the steroid and xenobiotic receptor, while the tocopherol did not bind or activate. Tocotrienol reduced the viability of pancreatic stellate cells (play a pivotal role in the development of pancreatic fibrosis), while alpha-tocopherol did not. Although tocopherol did not block glutamate-induced death, alpha tocotrienol did. Experimental studies show that Γ-tocopherol is superior in detoxifying nitrogen dioxide, γ-tocopherol is almost as potent in anti-oxidation properties compared to α-tocopherol, and its properties in detoxifying electrophiles are superior. Tocotrienols seem to be superior compared to tocopherol because of their better distribution in fatty layers of the cell membrane.

Conclusion

This work tries to show that, although alpha-tocopherol saturates the tissues, blood plasma, and the αtpp, and stays in the blood longer, does not mean that the other vitamers do not have activities. Studies presented show that especially the tocotrienols, seem to outperform the alpha-tocopherol, and have different roles in the body.

Vitamin E (alpha-tocopherol) has been shown to be beneficial with experimental and animal studies, but so far clinical trials in heart studies involving humans are not that convincing. Meta-analyses show that alpha-tocopherol shows no reduction in mortality, cardiovascular death in diverse populations, or even may increase all-cause mortality(although other studies report that up till 400 IU per day shown no harmful effects). Despite these studies, alpha-tocopherol seems to be noted as being active in textbooks. The other 7 tocopherols and tocotrienols show as much promise as alpha-tocopherol does. 95% of all vitamin E studies are focused on alpha-tocopherol giving an impression about vitamin E superiority that leaves the other vitamers unexposed. One possible reason that alpha-tocopherol may be harmful with supplementation is the depressing properties of alpha to other forms of vitamin E. The difficulty of assessing and comparing the bioactivities of alpha-tocopherol versus the rest is the potential other activities and functions of the tocopherols-and-trienols. After reviewing multiple studies, my conclusion tend to sway towards activities of multiple forms of tocopherol and tocotrienols besides alpha-tocopherol. The limitations of the other forms of tocopherol are clearly there (especially transport, bioavailability) but this can be overcome. In clinical nutrition, a functional approach, the bioavailability is named in percentages, these percentages are based on rat studies. Following that logic, vitamin E alpha-tocopherol should be protective against heart disease in humans by its protective functions in rats.

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