Previous studies examining this issue have largely focused on individual functions/symptoms or genes using relatively small sample sizes. Here we took a systematic approach, and examined the entire genome using large GWAS datasets and multiple traits. We observed different patterns between the reciprocal polygenic analyses (comparing Tables 1 and 2). When we used the genetic risk scores of schizophrenia to predict ND traits, the association was evident at P-values ≥ 5 × 10−3, with the association strength increased as the P-value threshold became larger (Table 1). Given that the PGC schizophrenia GWAS did not control for smoking status and quantity, and there was a large difference of smoking prevalence between schizophrenia patients and controls (on average, 65% or more schizophrenia patients smoke, and about 20% people smoke in the general population), we would expect that the PGC schizophrenia GWAS identify top candidates for ND related traits. But what we found was not the case. These top ranked candidates (i.e. those with P-values ≤ 5 × 10−5) from the PGC schizophrenia meta-analysis1 were not predict ND related traits. A likely explanation
