A novel approach to modeling tissue-level activity of cortisol levels according to the theory of Endobiogeny, applied to chronic heart failure

Background: Chronic heart failure (CHF) is an inflammatory disorder in which cortisol plays an important role. Despite this, cortisol is not routinely quantitatively measured for a number of reasons. It is considered non-specific. Accuracy and validity remain in question. It is not considered convenient or cost effective. Finally, tissue level effects of cortisol do not correlate linearly to quantitative levels. If the functional, tissue level effectiveness of cortisol could be modeled, its evaluation in CHF patient may become relevant. Endobiogeny is a global systems theory that claims to be able to model complex physiology through biomarkers, offering context-rich interpretations of data for meaningful clinical applicability. Cortisol is known to alter circulating levels of elements from a complete blood count (CBC). By relating these biomarkers in a qualitative fashion, the theory of Endobiogeny posits that these elements can be contextualized to reflect the tissue level activity of cortisol, referred to as the cortisol index (CI). The algorithm derived from the theory is called the Biology of Functions (BoF). Aim: The aim of this study was to determine if the cortisol index is accurate in reflecting a greater expression of cortisol activity in ambulatory CHF patients versus controls subjects. Methods: A retrospective observational case control study was performed in 93 patients with New York Heart Association class II-III heart failure patients and 104 individuals with no cardiovascular pathology as a control group. Results from a CBC were entered into BOF modeling software, from which the cortisol index is derived. Results: The Cortisol index (3-7) was significantly elevated in CHF vs. control patients (12.8±0.91 vs. 8.48±0.74, p< 001), as were individual CBC elements used to form the index. Conclusions: The cortisol index, derived from the theory of Endobiogeny showed results consistent with CHF pathophysiology. The cortisol index was able to model the effective tissue level activity of cortisol in CHF patients using only a CBC, without measuring serum cortisol. Future studies should compare the cortisol index to standard inflammatory markers in CHF patients to further correlate the validity of the index to other known effects of cortisol.