Mathematical simulations demonstrate that elevated alcohol intake is significantly associated with the development of hypercortisolism and disruptions in HPA axis function and circadian rhythm.
Does simulated alcohol consumption disrupt HPA axis dynamics and lead to hypercortisolism in a mathematical model?
Mathematical modeling demonstrates that elevated alcohol consumption can disrupt HPA axis dynamics and circadian rhythms, potentially leading to hypercortisolism.
Abstract In this study, we develop a mathematical model to examine the effects of varying levels of alcohol consumption on the dynamics of the hypothalamic-pituitary-adrenal (HPA) axis. Our model also integrates circadian and ultradian rhythms to more accurately represent physiological responses over time and explores age and gender related impacts on HPA axis function. Despite the omission of gonadal hormone-cortisol interactions and other simplifying assumptions that had minimal influence on outcomes, simulation results reveal a significant association between elevated alcohol intake and the development of hypercortisolism, or Cushing’s syndrome, underscoring potential disruptions in HPA axis function and circadian rhythm behavior induced by alcohol. These findings underscore the importance of understanding the influence of external factors such as alcohol on stress regulation and provide new insights into the pathophysiology of stress-related disorders.
Gergley et al. (Thu,) conducted a other in Hypercortisolism. Alcohol consumption vs. No alcohol consumption was evaluated on HPA axis dynamics (cortisol levels). Mathematical simulations demonstrate that elevated alcohol intake is significantly associated with the development of hypercortisolism and disruptions in HPA axis function and circadian rhythm.