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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Circ Cardiovasc Genet. 2016 Oct 26;9(6):495–503. doi: 10.1161/CIRCGENETICS.116.001457

Table 2.

Statistically significant GRS interactions with baseline adjusted 1-yr traits (Nmax=1,377)

Trait GRS Intervention
arm
N β SE P 95% CI LL 95% CI UL Pinteraction
large HDL
(μmol/l)
large HDL GRS Placebo 463 −0.022 0.032 0.499 −0.086 0.042 -
large HDL
(μmol/l)
large HDL GRS Metformin 461 −0.075 0.034 0.027 −0.141 −0.008 0.07
large HDL
(μmol/l)
large HDL GRS Lifestyle 450 −0.111 0.039 5×10−3 −0.188 −0.033 1×10−3

95% CI LL - 95% confidence interval lower limit; 95% CI UL - 95% confidence interval upper limit; β - beta effect estimate per GRS risk allele; DPP - Diabetes Prevention Program; HDL - high density lipoprotein; GRS - genetic risk score; N - sample size; SE - standard error.

P values are based on linear regression models. GRS associations were modeled by fitting the GRSs as the independent variables with the different lipoprotein subfractions as dependent variables.

Pinteraction values are based on linear regression models. GRS associations were tested by fitting the GRS × lifestyle vs. placebo intervention and GRS × metformin vs. placebo intervention interaction terms as the independent variables with the different lipoprotein subfractions at follow-up as dependent variables. β coefficients reflect the association of one genetic risk score unit (effect allele) with the trait (expressed in native units and inverse normalized units).

Age, age2, sex, baseline lipoprotein subfraction values and genomic principal components were used as covariates in all models.