Page 9 - GPD-2-3

Gene & Protein in Disease Albumin (HSA) binding and health

within narrow limits and any deviation from normal the body bound, with the most abundant binding protein
blood flow or ability to bind ligands will decrease nutrients being HSA. Sites of nutrient production are linked to
in the HSALNP and cause albumin-binding deficiency targets so that sufficient nutrition is constantly maintained
(ABD) with corresponding changes in nutrients, colloidal as in the regulation of glucose. Both the HSALNP and ABD
pressure, and diastolic pressure. Nutrients travel around are a logical explanation of the processes that must exist to

Figure 2. The human serum albumin lymphatic nutrient pump.

• Hypoalbuminemia is a known factor in sepsis patients [15-18] and COVID-19 .
[18]
• Hypoalbuminemia is associated with inflammation [18-21] and is a marker for checkpoint blockade .
[22]
• Insulin production is a known determinant of HSA .
[23]
• HSA is implicated in recovery from post‑cardiac arrest and coronary heart disease :
[24]
[25]
• It is a useful predictor of ketoacidosis [26,27] .
• Since early 2020, researchers have been reporting the relationship between COVID‑19 and both intravascular HSA levels and hypoalbuminemia [28-38] .
• Albumin oxidation in COVID‑19 is known to occur as is structural damage and glycogenesis , in each case HSA binding is decreased.
[37]
[39]
[38]
• Binding of ligands affects HSA levels: HSA binds to the COVID‑19 spike 1 subunit and predicts in‑hospital survival .
[40]
• The progress of HSA in sepsis and COVID‑19 has been evaluated and oxidative stress is known to occur during HSA deficiency .
[39]
[38]
• HSA levels may identify patients with SARS‑CoV‑2 infection in whom inflammatory processes are occurring and serve as a potentially useful marker
of disease severity and prognosis [29-33] .
• The existence of a mechanism, through the HSALNP that explains the kinetics of serious COVID‑19 vulnerabilities, such as ABD, is described here.
• HSA is self‑regulated through feedback from pressure within the hepatic portal vein – 80% of this pressure is from HSA.
• HSA is therefore the primary determinant of body fluids as all other mechanisms of the blood regulate around this changing concentration.
• In the 19 century, earnest starling investigated the effects of colloidal pressure on capillaries and understood that HSA as the primary colloid was the
th
determinant of WBF [13,14] and noted the effect of colloids on nutrition. Starling understood the relationship between colloidal pressure and diastolic pressure.
Figure 3. Evidence that vulnerabilities and sepsis in COVID-19 are caused by human serum albumin (HSA) binding deficiency. Based on the evidence
presented here, the regulation of HSA levels forms the basis of mean cardiovascular return and output when the body is at rest, with systolic/diastolic
pressures being optimal. Any lowering of pressure causes production of HSA and an increase in plasma volume. Glucose and ketones are then corrected at
this level as are other nutrient ligands, according to their own mechanisms.
Volume 2 Issue 3 (2023) 3 https://doi.org/10.36922/gpd.0328