Background: This article follows a theme of articles on the subject of
‘neuroregulation’ published by the author. The aim of this original article is to further
elucidate that ‘Blood Glucose is Neurally Regulated’, in particular, that type 1 and
type 2 diabetes are co-morbidities because the genetic expression of insulin is
followed by the reaction of insulin with its substrate; and that any explanation for
type 1 and type 2 diabetes must conform to the fundamental laws of chemistry which
govern chemical reactions and influence (i) how the protein is expressed or activated
(genotype) and to what extent, (ii) how the protein maintains its shape and reactivity
(phenotype), (iii) how the protein reacts with its substrate, and (iv) that there is a
complex network of organ systems which regulate functional parameters such as
blood pressure, blood glucose, acidity, etc.
It considers that the regulation of blood glucose, which we recognise as type 1 & 2 diabetes, is heavily
influenced by the neural regulation of pH. In addition, recognition that the brain regulates the autonomic
nervous system and physiological or functional systems leads us to consider that the onset and
progression of type 1 diabetes, and hence the expression of pre-pro-insulin, are influenced by the many
and various factors which alter gene conformation, the genetic expression of proteins, protein
conformation, and/or by associated chemical reactions e.g. resulting from the influence of viruses,
vaccines, drugs, bacteria and stress.
Conclusions: Finally, and in support of the arguments presented, this article reports how Strannik
Virtual Scanning – a cognitive technology which encompasses an understanding of the structural nature
of the relationship between brain function, autonomic nervous system, physiological systems and
pathological correlates - is able to distinguish between prediabetes and diabetes, between genotype and
phenotype, determine the complex range of emergent pathologies influencing the health of each and
every organ, and contribute to further advances regarding diabetes etiology.