A train of oxidative consequences - manganese and Sjogren's

Here is the follow-up to the post I wrote last time on the tackling of extreme tiredness, a typical symptom felt by Sjogren's syndrome's patients. Remember I did link it to the 'greedy' metabolism of folic acid and vitamin B12 (HERE), triggered by the spiral-shaped bacteria Helicobacter pylori. If you remember there was still a bit of a bridge to build in order to establish a better understanding of the whole chain of consequences. I could not immediately understand how we could go from high homocysteine levels to a manganese deficiency (see diagram on referred post).

OK, but just for the sake of remembering exactly what was mentioned, let me produce a 'train' of consequences hereby:

H. pylori is responsible for the chronic degenerative gastritis -> that results in low plasma levels of folic acid and vitamin B12 -> with produced consequences to our 'chromosomal health' -> responsible for the elevated homocysteine levels (possibly linked to a defective participation of the enzyme methylenetetrahydrofolate reductase responsible for hyperhomocysteneimia) [1] -> resulting in chromosomal imbalance and genotoxicity.

But what is in fact the impact of elevated homocysteine levels in the human blood plasma that is likely to induce a serious reduction in the manganese levels? And what real impact does this manganese deficiency have on patients suffering with Sjogren's syndrome?

Very well! For the bacterium to establish itself in our gastric environment it will have to face a very acidic challenge, i.e., the neutralisation of the gastric juices. And how is this done? By releasing enzymes (arginase and subsequently urease) into the acidic moiety that use up the second-favoured metal co-factor manganese (when cobalt is not readily available) [2]. As simple as that! And that is the primary action that will determine a manganese deficiency in our system. That, alongside the prior folic acid and vitamin B12 reduction (also especially correlated to high homocysteine levels 'in men' as suggested by [3]), complement a very particular and aggressive attack to biochemical 'energy' determinants. Affecting exactly what? The mitochondria and the releasing of reactive oxygen species that will poison our body. Why? Because free radicals will negatively interact in random unexpected ways with numerous other important molecules throughout our organism [4].

With less manganese available the weaponry to detoxify our organism will be found deprived. Because manganese is a component of the superoxide dismutase that acts as a powerful antioxidant. This is why it is so important for those coping with Sjogren's syndrome to have a daily intake of around 30 g of walnuts. Because alongside omega-3 these nuts provide us with important manganese batteries.

There we go! Bridge created. We can now cross to the other side and 'recce'. In the coming Sjogren's syndrome post I will be disclosing my utter secrets on my favourite weaponry against the most limiting symptoms one can be affected with. I will bring a list of the finest guns for your protection and counterattack.

In the meantime and before I go, I must give 'kudos' to an impressive blog that helped me think through the processes when I got stuck in my scientific approach. I read a post that helped me establish this chain of events in a way that I found it so much easy to write after reading it. This is proof that there are very intelligent and dedicated science people writing for the common public these days. The blog I am referring to is called "Gutsy" and you can access it here. Apart from the excessive advertising and the cliché bible verses, said blog is very good indeed.

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A special thanks to the 'Gutsy' writer of the post:

THE REAL TRUTH ABOUT H. PYLORI: ALLERGIES, AUTOIMMUNE, & ADRENAL FATIGUE

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[1] Friedman, G., Goldschmidt, N., Friedlander, Y., Ben-Yehuda, A., Selhub, J., Babaey, S., Mendel, M., Kidron, M., Bar-On, H. (1999). "A common mutation A1298C in human methylenetetrahydrofolate reductase gene: Association with plasma total homocysteine and folate concentration". The Journal of Nutrition, 129(9), pp. 1956-1961.

[2] Azizian, H., Bahrami, H., Pasalar, P., Amanlou, M. (2010). "Molecualr modelling of Helicobacter pylori arginase and the inhibitor coordination increases". Journal of Molecular Graphics and Modelling, 28(7), pp. 626-635.

[3] Lussier-Cacan, S., Xhignesse, M., Piolot, A., Selhub, J., Davignon, J., Genest, J. (1996). "Plasma total homocysteine in healthy subjects:sex-specific relation with biological traits". The American Journal of Clinical Nutrition, 64(4), pp. 587-593.

[4] Halliwell, B. (1991). "Reactive oxygen species in living systems: Source, biochemistry, and role in human disease". The American Journal of Medicine, 91(3-3), pp. S14-S22.