Magnesium Therapy Prevents Senescence with the Reversal of Diabetes and Alzheimer’s Disease

Abstract

In the current global epidemic for Non Alcoholic Fatty Liver Disease (NAFLD), diabetes and neurodegenerative diseases such as Alzheimer's disease there has been a major interest in magnesium therapy to delay the severity of NAFLD, Type 3 diabetes and neurodegeneration in the developing and developed world. The objective of magnesium therapy is to activate the anti-aging gene Sirtuin 1 (Sirt1) to prevent cardiovascular disease, NAFLD and diabetes. Reduced consumption of nutrients such as fatty acids, glucose, cholesterol and increased magnesium consumption is closely linked to reduced bacterial lipopolysaccharides (LPS) and activation of Sirt1 relevant to active nuclear and mitochondria interactions with the prevention of myocardial infarction and Type 3 diabetes. Magnesium deficiency and its effects on Sirt1 regulation have become important with magnesium deficiency associated with appetite dysregulation, senescence, glucose/nitric oxide dyshomeostasis, increased ceramide and toxic amyloid beta formation. Magnesium therapy activates the peripheral sink amyloid beta clearance pathway with the reversal of cell senescence associated with various chronic diseases such as cardiovascular disease, Type 3 diabetes and Alzheimer's disease.

Nutrition Therapy Regulates Caffeine Metabolism with Relevance to NAFLD and Induction of Type 3 Diabetes

“…Sirt 1 regulation of SCN synchrony and neuron synapse plasticity is completely corrupted by caffeine as caffeine overload in the CNS occurs with aging process. Magnesium deficiency is connected to endothelial dysfunction [103][104][105], myocardial infarction [106][107][108][109][110], NAFLD [111,112] and the induction of T3D (magnesium/Sirt 1 activator) [113].…”

“…In the developing world alarm has been raised with the increase in plasma bacterial Lipopolysaccharides (LPS) levels with LPS [8,9,19,20,31,49] of relevance to Sirt 1 repression and associated with the development of insulin resistance and NAFLD. LPS may induce zinc [9] and magnesium [113] deficiency with LPS effects on zinc, magnesium and albumin levels relevant to increased free caffeine levels and linked to increased mitochondrial apoptosis in cells. The role of zinc/magnesium (Sirt 1 activators) deficiency in the developing world [146] may indicate Sirt 1 to be non-functional in the central nervous system and relevant to the induction of T3D.…”

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

“…Moreover, corresponding brain atrophy due to apoptosis in NRF1 deficient mice was observed [110][111][112]. Mutation in APOE4 that blocks NRF1 binding to the exon 4 of the gene has been recently linked to AD [113]. The Nuclear factor E2 (NRF2) is a master regulator which aids the expression of cytoprotective genes related to inflammation, mitochondrial biogenesis, antioxidant enzymes, and the proteasome pathway.…”

Heat Shock Gene Sirtuin 1 Regulates Post-Prandial Lipid Metabolism with Relevance to Nutrition and Appetite Regulation in Diabetes

“…supersede LPS inhibition of Sirt 1 [18,37] with prevention of defective cell transcriptional ontogeny and membrane transformations in the brain and liver [45,46]. Appetite dysregulation in diabetes may require these activators of Sirt 1 with relevance to the maintenance of neurons and the treatment of Type 3 diabetes with defective apelinergic system that involves thermo dysregulation.…”

“…In the developing and developed world diabetic treatment has become important with defective Sirt 1 gene expression determined by miR-34a [18,36] related to defective cell proliferation in the brain and the liver ( Figure 2). Defective thermoregulation may be relevant to ingestion of food (Sirt 1 defective)with inappropriate post-prandial lipid and amyloid beta metabolism that inactivate magnesium therapy that may now be relevant to HSP and amyloid beta metabolism with relevance to myocardial infarction [3,37].…”