However, the study is from Estonia, which has a significant prevalence of non-sanguine A and PA types. The “non-aggressive” Study Group -- by entanglement -- must be highly sanguine, and likely shows a difference in N trait between the Study Group and the Control Group, the latter having a significant proportion of aggressive non-sanguine A and PA types.
So, an excess of TT homozygotes in the Study Group could correspond to an excess of sanguinity in that group, which fits nicely since sanguinity is Mendelian recessive at the N locus (according to our model).
Also, one would expect the N locus to be related to the serotonin pathway, more so than the A locus, which has to shut off adrenergic expression and the A rage related to the sympathetic nervous system.
If the TPH2 rs4570625 gene turns out to be related to the N trait, then as usual one must keep in mind that it could be just a proxy for a nearby active site in linkage disequiblibrium, or part of a broader active haplotype.
So, this would be a good example of how entanglement between traits N and A can potentially cause confusion in the results of a case-control study.
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