This author puts out an excellent strategy best used when one is young and all their parts are working as they should. An excellent read, highly recommended. The paper is 50 pages long but he has close to 22 pages worth of references.
Free radicals generated at high rates under pathophysiological conditions are insufficiently detoxified by scavengers.
Despite some positive results in animal studies, the epidemiological and clinical outcome with conventional antioxidants such as ascorbate, tocopherols or carotinoids has remained relatively poor [1–5]. Although a sufficient supply with antioxidant nutrients is, of course, a prerequisite of healthy aging, a surplus of these compounds, given at elevated doses as food additives, does not seem to be a promising strategy, at least not as long as these substances are exclusively acting as radical scavengers. Moreover, pharmacological concentrations of some antioxidants can cause undesired effects, such as redox cycling or formation of toxic dimers or other secondary products.
However, a rise in radical formation should not only be seen as a cause of further damage, but also as a possible consequence of an otherwise initiated malfunction, e.g., by neuronal or cardiac overexcitation, calcium overload, ER stress, protein misfolding or reduced expression of relevant proteins which may end up in enhanced mitochondrial electron leakage. Consequently, attempts of reducing cellular radical generation should not only focus on proximate goals related to the sites of formation, but also try to identify and counteract the processes leading to the underlying primary dysfunction. Therefore, an approach of simply detoxifying radicals already formed cannot be sufficiently successful, so that radical avoidance in the broadest sense should come into focus.
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Neuroprotection by Radical Avoidance Search for Suitable.pdf 274.04KB
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