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Considering the notion has been raised that sub-clinical presentation of konzo exists, these measures may allow for the identification of individuals who show similar reduced antioxidant capacity as those with konzo, but who do not show a visible physical disability, enabling the overdue refinement of the clinical features associated with this disease 3,42

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Production of these reactive oxygen species is known to occur as a result of a few different mechanisms: 1) mitochondrial origin in which free radicals either escape scavenging enzymes or develop due to an error in oxidative processes, 2) inside the capillary endothelium where a hypoxic and reoxygenation process is created during intense exercise as well as during various types of cardiovascular disease, and 3) an oxidative burst from inflammatory cells which are commonly mobilized as a result of the muscle or tissue damage which is well-documented with extended or eccentric-based exercise[1]

Endocrine disruptors and obesity

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