| Abstract/Notes |
In concluding this review of the impact of suboptimal insulin and glucose metabolism on the brain and its tendency to lead to the development of amyloid beta (AB) and other adverse changes consistent to Alzheimer's Disease/senile dementia, is it enough to say that the relationship is a simple issue of aberrant insulin activity and too much or too little glucose? A recently published paper entitled "Molecular pathophysiology of impaired glucose metabolism, mitochondrial dysfunction, and oxidative DNA damage in Alzheimer's disease brain" by Abolhassani et al suggests no. If fact, according to the authors, the insulin mediated disturbances in glucose metabolism in the brain create damage through mechanisms briefly discussed in part VIII of this series, mitochondrial dysfunction and oxidative damage. Therefore, I would now like to expand my brief discussion on mitochondrial dysfunction and oxidative damange that I initiated in part VIII by providing some highlights from the Abolhassani et al paper. Before doing so, though, I would like to answer a question that you might have - Why is it necessary to have such a detailed understanding of the process? For me, the answer lies in the old saying: "Just because you pulled the knife out of the wound does not mean the wound will heal." What do I mean by this? It may be that optimizing insulin and glucose metabolism, which we, as nutritional and functional medical practitioners, have been doing very well now for decades, may not be enough from either a preventive or therapeutic standpoint. Why? I would suggest that long term disturbances in insulin and glucose metabolism will have a ripple effect creating collateral metabolic damage that will not self-correct once insulin and glucose metabolism is optimized. Instead, other complementary interventions not directly related to insulin/glucose metabolism may be required. Since, as suggested above, this "collateral damage" involves mitochondrial function and oxidative processes, these other complementary intervensions could take the form of other modalities we have successfully used for years to both mitochondrial function and reduce excessive oxidative activity.
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