Quantitative Simulation of Enzymatic Breakdown of Alcohol in Human Metabolism

The breakdown of ethanol, the active chemical in alcohol, is tightly regulated by the body, yet alcohol intoxication occurs in thousands of Americans annually. Many factors contribute to the concentration of ethanol in the bloodstream and the tolerance an individual has, including body size, previous drinking experience, and liver functionality. We propose a model that estimates both the blood alcohol concentration and the concentration of acetaldehyde (the toxic intermediate during catabolism) in the liver over time to quantify organ damage for an average person. From the current literature, we derived ordinary differential equations that govern the absorption of ethanol in the body and extended it with the metabolic enzyme mechanisms. We also altered the parameters of our system in order to show the effects of Asian flush, which impairs the body's processing of acetaldehyde. We demonstrated the accumulation of acetaldehyde in Asian flush patients was about 660 times higher compared to those without the disease.Clinical relevance—With further improvements and personalization, our model would be able to quantitatively describe the effects of alcohol consumption without having volunteers go through repetitive trials with extensive exposure to alcohol. Liver damage can also be estimated with the acetaldehyde buildup predicted by the model.