Alcoholism plays a major role in the insufficient utilization or deficiency of the vitamin B-complex molecules, and the pathologies resulting therefrom. Thiamine, pyridoxamine, and folic acid, each contain primary amine functional groups, whereas nicotinamide and vitamin B12 contain amide groups, each of which are potential reactants with acetaldehyde (AcH), the primary intermediate in the metabolism of ethanol. In this current study, it is reported that prothrombin time (PT), which is prolonged in a fraction of the alcoholic population, can be modified (in the laboratory) when several B-complex vitamins and AcH are added successively to human plasma or are premixed prior to the addition to plasma. Particularly, thiamine, pyridoxamine, and folic acid, at 0.01 mol/l, when added successively with 44.7 mmol/l AcH to plasma, or when premixed prior to addition to plasma, produced a marked reduction in the anticoagulant effect of AcH. Nicotinamide had no effect on PT nor did mixtures with AcH effect PT. However, NAD+, which contains a primary amine in its AMP moiety, reacted with AcH, lowering the latter's anticoagulant activity upon addition to plasma. Vitamin B12 did not affect PT. Interestingly, successive mixtures of vitamin B12 and AcH to plasma resulted in a small but statistically significant increase (P ≤ 0.05) in the anticoagulant effect of AcH, whereas premixtures had no statistically significant effect (P > 0.05). The decrease in anticoagulant activity of AcH in the presence of B-complex vitamins and NAD+ suggests that the primary amines in these molecules may form Schiff bases with AcH, thereby lowering both the free AcH concentration as well as the ability of the free vitamins/coenzymes to partake in essential physiological reactions.