Abstract

Diabetes is a Complex Neurological, Multisystemic, Multipathological, Polygenomic Disorder

Author(s): Graham Wilfred Ewing

Diabetes is commonly perceived to comprise two distinct processes commonly referred to as type 1 and type 2 diabetes. Each is considered to be a distinct process however difficulties continue to exist concerning the ability of current tests to diagnose diabetes with the result that patients may be misprescribed medication or may not need medication or would benefit from other interventions. The author illustrates that type 1 and type 2 diabetes exist as coexistential morbidities in which the type 1 condition is associated with the ability of a spectrum of genes to act coherently and express the insulin precursor pre-pro-insulin (genotype) and the type 2 condition is associated with the ability of insulin to react with its receptor protein (phenotype). Yet this does not entirely explain the phenomena of diabetes in which the brain regulates levels of blood glucose between upper and lower limits of typically 4-8mmol/l; or how pathologies in other organs and/or systems can influence blood glucose levels; or how changes of colour perception accompany pathological onset. So what is missing from current etiology? If there are changes of molecular biology (i.e. pathological onset) this must influence cell biology, organ function, and the coherent function of the organ networks (physiological systems). Moreover the GP’s consultation remains based upon a rudimentary and imprecise understanding of these physiological systems. So what are these physiological systems and why are they important? The function of the brain is to continuously monitor and optimise the body’s physiological stability i.e. to maintain physiological parameters between upper and lower limits. Each of these neurally regulated systems performs a distinct physiological function. In the regulation of blood glucose the most significant of these systems appear to be the optimisation of pH, sleep, and sexual function. Pathological onset and/or instability in these organ systems leads to multi-pathological and/or multi-symptomatic onset in other organs and organ systems e.g. leading to diabetes, hypertension, chronic kidney disease, circulatory problems, depression, Alzheimer’s disease, etc. So how can we measure such a complex phenomena in which pathological onset occurs across a spectrum of systems and organs? Changes of colour perception accompany the onset of diabetes as a result of the emission of biophotons as proteins decay to their unreactive state following pathological reactions resulting from stress, hyperindulgence, the consumption of acidified and/or alcoholic beverages, etc. Many companies have sought, invariably unsuccessfully, to adapt this phenomena perhaps because they have sought to make a simplistic association between changes of colour perception and diabetes rather than considering the complex nature of the association(s). The Human Brain Project was established to understand this phenomena, in particular: what the brain does and how it does it - it functions as a neuromodulator which continuously optimises the body’s physiological stability; to use such knowledge to develop a new generation of cognitive diagnostic with particular emphasis upon the diagnosis of complex medical conditions such as Alzheimer’s Disease; and to understand and adapt with therapeutic effect the multilevel nature of brain function. Such knowledge - for example as the Strannik Virtual Scanning test - has the capability to be able to screen the patient more effectively i.e. in far greater levels of precision and sophistication, than current tests; to establish the onset of diabetes and diabetic comorbidities; and at lower cost, perhaps significantly so. Moreover, the understanding of the relationship between sense perception, brain function, the autonomic nervous system and physiological systems, and pathological onset; has significant therapeutic potential.


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