The morbidity first affects organs belonging to the visceral compartment: hepatic steatosis [19] causing decreased synthesis of liver-secreted protein markers, notably serum-albumin (Alb) [20], transferrin [21], TTR [22], retinol-binding protein (RBP) [23], and insulin-like-growth factor 1 [24]; involutional flattening of the intestinal mucosa [25] which is responsible for malabsorptive syndromes; and a drastic decline in immune capacities [26], rendering these patients highly vulnerable to superimposed infections. Here, ALB is linked to fatty liver disease.