Epidemiological Study Shows Correlation Between Anti-Oxidant Intake and C-Reactive Protein & Homocystein

After a sudden onset of discussions around the beneficial or even detrimental effects of vitamin supplements in general and antioxidants in particular in the mid to late 2000s, vitamins and, even more, other anti-oxidants have been put back on the map, lately.

A recent epidemiological study from the University of Connecticut (Floegel. 2011) provides further evidence for the hypothesis that, after all, consumption of adequate amounts of vitamins C and E, beta carotene, flavonoids and selenium would be beneficial to your overall health

Intakes of vitamins C and E and carotene were inversely associated with the probability of having serum CRP concentrations >3 mg/l in multivariate logistic regression models. Flavonoid and Se intakes were not associated with the odds of elevated serum CRP concentrations. The mean plasma Hcy concentration was 8·61 (95 % CI 8·48, 8·74) μmol/l. Intakes of vitamins C, E, carotenes and Se were inversely associated with the odds of plasma Hcy [Homocysteine] concentrations >13 μmol/l after adjusting for covariates

While all these results appear to be quite unambiguous, you still have to keep in mind that they support the interpretation "antioxidants are healthy" only, if we assume that the relation between high C-Reactive Protein [CRP], inflammation and the metabolic syndrome, as well as the relation between homocysteine and heart disease is more than just a correlative one; and, to my best knowledge, no study has yet been able to show that injection of homocysteine caused heart disease or an increase in CRP increases inflammation or causes tissue damage. In this context, for example, the hitherto hardly understood involvement of "positive inflammation", such as an exercise induced rise in IL-6 levels, come to mind. In this context, studies such as Ristow et al. (2009) that found the positive effects of exercise being blocked by antioxidant supplementation would warrant further research into what - irrespective of reductions in purported markers of inflammation and cardiac disease - the actual health outcome of higher antioxidant intakes are.


Note: Don't get me wrong. I do not want to argue against a diet rich in natural antioxidants. I just want YOU to be aware that the proven health benefits from eating healthy, antioxidant-rich foods cannot be extrapolated to high (or even mega-dose) vitamin & flavonoid supplements and that taking megadoses of isolated antioxidants such as alpha-tocopherol (especially in its synthetic form and without the complementary tocopherols and -trienols), which is the most commonly sold form of vitamin E, may in fact do more harm than good.

ALA + Vitamin E Make Up for Fructose Induced Cardiovascular and Metabolic Changes

Alpha Lipoic Acid (ALA) and vitamin E are among the most investigated and best-known natural antioxidants. And, despite the fact that scientists came to realize, that both, ALA as well as alpha-tocopherol, are far from being the saviors of the metabolically deranged, they were once hailed as, a recent study from the University of Queensland (Patel. 2011) demonstrates their therapeutic potential in an animal model that (unfortunately) is not far from the high fructose corn syrup fed morbidly obese man/woman in a western(-ized) society.

Patel et al. found that supplementation with vitamin E (either α-tocopherol or tocotrienol-rich fraction, 0.84 g/kg food) and α-lipoic acid (1.6 g/kg food) could prevent (high fructose diet + Vit E + ALA) and even reverse (Vit E + ALA after high fructose diet for 8 weeks; reversal protocol) "glucose intolerance, hypertension, and increased collagen deposition in the heart together with an increased ventricular stiffness" in rats fed a high fructose diet over a course of 16 (prevention) / 8 + 8 (reversal) weeks.

Figure 1: (a): Plasma glucose concentrations following oral gavage of glucose (2 g/kg) recorded after 16 weeks for rats fed with corn starch (⬤), fructose (⚪), or fructose with α-tocopherol and α-lipoic acid as either prevention (FTPP) (▲) or reversal (FTPR) (▾) protocols. (Patel. 2011)

As a faithful visitor of the SuppVersity, you probably won't be surprised to read that supplementation with a tocotrienol enriched vitamin E source produced even more favorable outcomes in terms of blood glucose (5.0 vs. 6.4mmol/L in the prevention groups) and the other markers of metabolic health. It should not astonish you, anyway. It's no coincidence that nature provides us with certain nutrients in certain ratios and isolated alpha-tocopherol is something you won't find in nature...

And again: Vitamin E Supplementation has no Effect on All Cause Mortality

I suppose, only few of you will be surprised to read this: A very recent review by scientists from the University of Kentucky (Abner. 2011) confirmed the results of previous reviews of the available literature:

Based on the present meta-analysis, supplementation with vitamin E appears to have no effect on allcause mortality at doses up to  5,500 IU/d.

The scientists had compiled a selection of randomized, controlled trials published between 1988 and 2009 that investigated the treatment effect of vitamin E supplementation in adults for at least one year. What they got was a data pool comprising 246,371 subjects and 29,295 all-cause deaths with an overall risk ratio of 1.00 that was independent of whether or not the subjects received supplementary vitamin E.

On a side note: Instead of another review of the literature, I would have liked to see a study investigating the differential effects of the various forms of tocopherols and tocotrienols, of which I assume that the interaction / ratio between those is where the magic happens. So, if you happen to own a big laboratory and do not know what to do with it, I would certainly post the results of such a study ;-)

Rat Study: High Carb Diet Induces Hepatic Steatosis and Increases Heart Fat by 43%

For a large part of the 1980s and 1990s fats have been considered the "source of all evil". Now, it is our carbohydrate consumption which is held to be responsible for diabetes, obesity and the other ugly faces of "the metabolic syndrom". A recent study by a group of scientists from Sao Paulo (Haubert. 2010) seems to confirm this "revised" hypothesis.

Over a period of 21 days, the scientists fed a group of rats (experimental) a 70% carbohydrate diet with astonishing or rather shocking results (cf. table 1)

 

Within three weeks the rats developed a fatty liver and their heart fat mass increased by 43%. While the scientists did not provide much information about the overall underlying mechanism of these changes, they emphasize the pronounced decline in tissue vitamin E produced by the high carb consumption. In how far additional vitamin E may have prevented some of the fat accumulation yet remains unknown and would warrant further investigation.

Vitamin E Exerts Positive Effects on Various Health Markers in Recreational Trainees

A study from scientists from the Azad University in Iran (Naghizade. 2010) shows that supplementation with 500mg vitamin E (~750IU) over a period of 8 weeks improved malondialdehyde (MAD, p<0.02) , creatine phosphate (CP, p<0.04), total antioxidant capacity (TAC, p<0.03), LDL (p<0.03) and Vo2max (p<0.03) over placebo values in moderately aerobically trained individuals:

In summery performing moderate aerobic exercise (HRmax 60-65%) with consumption Vitamin E may decrease membrane damage and lipid peroxidation, and cardiovascular risk factors.

These results stand in line with several other papers that have been released within the last months. Many of these found positive effects of vitamin E on moderately (mostly aerobically) training trainees, like the ones in this studies. If, however, the workloads increase way beyond the 3x45min (per week) the male subjects of this study spent in the gym, the results become equivocal and some studies even suggest that additional anti-oxidant supplementation may suppress positive adaption processes.