Control of mortality by human serum albumin

In a fit, resting human, efficient heart function depends on sufficient return of blood to the heart. At any stage of acclimatization, whether through changes in external environment or illness, pressures in the cardiovascular system must equilibrate to ensure adequate supply of nutrients to the deep capillaries, simultaneously providing adequate osmotic pressure to the cells and systemic pressure for venous return. About 80% of colloid osmotic pressure (COP) is controlled by levels of human serum albumin (HSA), which is the ultimate, homeostatic determinant of fluid volume (FV) in all compartments of the body and is controlled by the liver. The state of cardiovascular output is regulated by COP, which is determined by HSA colloidal pressure, which has clinical significance in many areas of medicine. In COVID-19 and other diseases like Streptococcus, where albumin binding has been suspected of being in deficit, we suggest that raising available HSA binding will alleviate vulnerabilities to disease and sepsis, unlike present forms of fluid therapy (FT). In this review, we describe how HSA binds and delivers nutrients as an intermediary transporter as it circulates, being especially important in the lymphatic system. Insufficient HSA nutrient binding leads to cell stress and albumin-binding deficiency (ABD) as both colloidal pressure and nutrients change lead to symptoms of sepsis. HSA binding can be reduced because of a lack of HSA or external ligands taking up binding sites on HSA. FV also affects long-term metabolic and cardiac diseases due to incorrect pressure and nutrients. The HSA lymphatic nutrient pump therefore utilizes HSA as an intermediate transporter of nutrient and waste ligands, and their circulation is determined by the lymph rather than the cardiac output. An elevation of the whole body colloidal pressure will increase the whole body FV and subsequently trigger production of all other nutrients in blood plasma and lymph: For example, body fluid increase will decrease blood oxygen to the kidneys promoting erythropoietin release culminating in the creation of new blood cells. We provide evidence that the hepatic portal vein (HPV) is essential in the precise control of HSA, glucose, and ketone metabolism and that the HPV is the appropriate target for FT and glucose control. We propose that in a clinical situation where this method is applicable, raising HSA will alleviate the symptoms of ABD and decrease the likelihood of serious illness and death by sepsis.