The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
part of the genetic heterogeneity among different people is the the apo lipoprotein a isoform size so uh people express uh different lpa isoforms some some are bigger than uh than the other and that that probably uh that well that actually plays an important part of the uh equation explaining why some people have a higher lp a little late than others
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it's been shown uh that um that the the children you can uh they have uh a very different lpa levels than than their uh than their uh mothers and fathers and you cannot really estimate it so you really have to to measure it
so the pattern of inheritance is true autosomal dominant uh pattern of inheritance so uh it's like any uh like for instance if you compare it with a monogenic disorder let's say familial hypercholesterolemia
because there's 2 000 different variants in the lpa region that are associated with high lpa so your father can have a high lpa because of a specific variant and your mother can have an lpa variant that lowers lpa but it depends on the combination of snips that you will ultimately get so it's not uh it's not as clear as any monogenic disorder even though it's a dominant mode of of inheritance