A Neurological Perspective upon Diabetes and Obesity, What They Are, and How They Can Be Measured

Abstract

New technologies bring new insights. The existence of the first mathematical model of how the brain regulates the autonomic nervous system and physiological systems, and knowledge of how this can be applied to screen or treat the diabetic, enables the author to take a comprehensive view of the etiology of diabetes and obesity. This paper illustrates the dynamic relationship between the brain, physiological systems and visceral organs. It highlights that 1) blood glucose is a neurally regulated physiological system, and/or network of organs, which function coherently in order to maintain blood glucose within normal physiological limits; and 2) that dysregulation of this physiological system (regulation of blood glucose levels), by genetic or phenotypic pathologies in the organs in this system, influences the prevailing levels of insulin, directly influences brain function and hence the coherent function of this and other physiological systems and organs e.g. blood pressure, sleep, pH, digestion, sexual function, etc. In addition 3) the observation that proteins may be coiled and reactive, or uncoiled and resist reacting with their reactive substrates, leads to a greater level of understanding of the mechanisms responsible for type 2 diabetes and obesity and how such conditions could be screened and treated.

A Discussion of the Current Limitations of Diabetes Etiology

“…Moreover the evidence for such a conclusion, and its relevance to how we screen or treat diabetes is already evident in various diabetes papers which illustrate that (i) changes of blue-yellow colour perception accompany the onset and progression of diabetes, (ii) that this phenomena is not unique to diabetes but can be used to screen for an extensive range of pathologies [38] including diabetic comorbidities, (iii) that the phenomena is associated with the emission of biophotons, (iv) that the vagus nerve is involved in diabetes etiology, (v) that insulin is released by the pancreas in a pulsatile manner which is indicative of 'control circuitry' , and (vi) that knowledge of this 'neuro-regulatory mechanism' can be used to treat patients with a wide range of pathological indications [39] including type 1 and type 2 diabetes and related diabetic comorbidities e.g. by reducing exposure to stress [30,58].…”

“…Ewing recognised that these fundamental objectives had been completed by Grakov in the period 1981/2-1997-2006 and were incorporated into the Strannik software. Papers followed which compared the two different techniques [33,34]; identified fundamental limitations of the techniques being deployed to achieve such objectives [34,35], in particular the reliance upon 'big data'; determined that the brain acts as a neuromodulator [36] of the autonomic nervous system; that Grakov had developed a screening test which can screen for the complex pathological correlates of diabetes and diabetic comorbidities including Alzheimer's Disease [37][38][39][40][41][42]; and had understood how this led to an understanding of the multilevel nature of brain function in particular of the mechanism which regulated the stability of the autonomic nervous system and the coherent function of the physiological systems [43].…”

Is Metformin a Drug or a Buffer and why is this Significant? Further Evidence that the Brain Regulates the Autonomic Nervous System, in Particular Prevailing Levels of Intercellular pH

“…blood glucose, HbA1c. Their insulin resistance (and also leptin resistance and ghrelin resistance) [32] will decline and they will have more normal appetite and satedness, and be less hungry. This highlights the need for a more complete and rigorous scientific understanding of how the body regulates its functions [103] which can be applied to improve the quality of healthcare and thereby reduce misdiagnoses, misprescribing of drugs, unnecessary prescribing of drugs, etc.…”

“…Every medical condition must therefore, to some extent, comprise a combination of genotype and phenotype. Accordingly, the diagnosis and measurement of diabetes and diabetic comorbidities should determine whether pathological onset in any of these and/or other systems and organs materially contributes to unstable or abnormal blood glucose levels [32].…”

“…That a particular protein reacts with another protein or substrate ignores the complex range of factors which influence this process and determine the rate at which this reaction proceeds e.g. pH, levels of essential minerals, the coiled or uncoiled nature of proteins [32], and their reactive substrates, etc;…”