Comparing a Type 2 Diabetic to Non-Diabetics’ Blood Glucose Levels

A statistical approach to modeling Medical Time Series (MTS) using Blood Glucose Levels (BGL) is provided, for the purpose of inferring the characteristics of control theory feedback & feedforward mechanisms underlying Type-II diabetes (T2D). From this perspective, the multiple mechanisms identified may then be related back to the known pathways of T2D in further studies for their probative value in establishing the dominant process(es) in blood glucose level (BGL) dysregulation. This study identified several BGL regulatory characteristics as stable statistical distributions. When non-diabetics’ (ND) BGL is compared to the BGL of a T2D patient with Multiple Sclerosis (MSD), this preliminary study identifies a lack of ‘Fine Control’ and a lack of ‘Gross Control’ of BGL. Fine Control is the rate of change of BGL within ±2.75 mg/dL/min and Gross Control is when this rate of change is > |30.0| mg/dL/min. In ND, the BGL probability distribution is Gamma (α = 43.3663, β = 10.9212), confirming BGL control/regulatory processes that maintain the normal BGL range. This Gamma establishes a characteristic sensitivity and responsiveness of ND BLG regulation based on a sample of 201 ND patients which can be used as a reference for other studies. In the sample T2D patient, the BGL probability distribution is also Gamma (α = 10.921, β = 12.4693) but has lowered mode, a distribution that is widened and shifted toward high glucose. Inferred from this change in Gamma is a lowered ‘sensitivity’ to small decreases in BGL demand, compared to the ‘sensitivity’ to small increases in BGL demand, identifying a ‘sensitivity asymmetry’. This small difference in ‘sensitivity’, and therefore in the body’s BGL regulatory response, is shown by simulation to produce sustained high BGL. Sensitivity in this context does not imply a dominant pathological or regulatory mechanism in T2D but is a statistical characterization of T2D. Therefore, the statistical sensitivity does not by itself distinguish between histological defects, such as for example the fate of pancreatic beta cells, and non-histological factors, for example the impact of SNO-CoA-assisted nitrosylase. A diurnal property of BGL was identified. BGL is either in an insulin dominance phase or a glucagon dominance phase, with macro level insulin dominance between 8:30 pm to 6:30 am and macro level glucagon dominance between 6:30 am to 8:30 pm. At the micro level this phase dominance is observed in the periods between measurements.