MAGNESIUM DEFICIENCY AND INDUCTION OF NAFLD AND TYPE 3 DIABETES IN AUSTRALASIA

Chronic diseases in Australasia 1 have attracted interest by medical researchers with relevance to the gene-environment interaction that indicates that genes under nutritional regulation have malfunctioned with the induction of organ suicide. The individuals in these communities develop appetite disorders 2 with consumption of excess food that leads to metabolic dysfunction, non-alcoholic fatty liver disease (NAFLD) and neurodegeneration. The organ that has central control of other organs is the brain and with brain neurotoxicity peripheral glucose levels increase and induce oxidative stress that leads to organ disease and brain disorders such as Type 3 diabetes 3,4 relevant to the apoptosis of cells in various tissues and organs. The role of anti-aging genes in Type 3 diabetes 2 has become of central interest to maintain mitochondrial functions and the identification of longevity genes that determine their function is critical to the prevention of chronic diseases in the developing and developed world. Mitochondria in neurons become unstable with neuron apoptosis 5–7 associated with accelerated aging. Neurons within the brain that regulate appetite become altered with altered gene expression and posttranscriptional regulation closely connected to overeating, defective post-prandial lipid metabolism and chronic diseases.