41 58 59 79 80 82 Several mechanisms such as inherited susceptibility, uterine environment and shared environment have been suggested for this familial aggregation pattern.
Susceptibility to environment has been previously reported for the H19 gene whose expression in mouse zygotes could be experimentally manipulated by in vitro culture conditions [31] and for reprogrammability of somatic nuclei in mouse clones [32].
It represents not only genetic susceptibility, shared environment, and common lifestyles, but also the interactions among them.
This concept is also more broadly relevant to other human diseases in which polygenetic susceptibility and environment interact.
Family history is an important risk factor that reflects inherited genetic susceptibility, shared environment, and common behaviors.
Complex interactions between genetic susceptibility and environment, influencing the immunological compartment during the prodromal period, lead in some individuals to overt immunological abnormalities, including occurrence of autoantibodies and islet-reactive T cells [ 5, 6].
Furthermore, genetic correlations for bTB susceptibility between environments that differed in herd prevalence of bTB ranged from 0.06 to 0.86 and were all different from one.
Consistent with this view, it is becoming increasingly evident that individuals differ in their susceptibility to the environment, both negative and positive, such that susceptible (malleable) individuals are more strongly affected for better and for worse [35], [36].
DNA, besides acting as this blueprint, can also provide us with information about our phylogeny, ancestry, environment, susceptibility to disease, and some claim our character and possibly our fate.
