For a long time, the origin of RHD polymorphism was an evolutionary enigma.[39][40][41] Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in a population of RhD positives or RhD-positive men in a population of RhD negatives) were at a disadvantage as some of their children (RhD-positive children born to preimmunised RhD-negative mothers) were at a higher risk of fetal or newborn death or health impairment from hemolytic disease. It was suggested that higher tolerance of RhD-positive heterozygotes against Toxoplasma-induced impairment of reaction time [36][37] and Toxoplasma-induced increase of risk of traffic accident[38] could counterbalance the disadvantage of the rarer allele and could be responsible both for the initial spread of the RhD allele among the RhD-negative population and for a stable RhD polymorphism in most human populations.