Since 25(OHD, PTH and calcium may act via mediating effects and/or be part of the same causal mechanism we considered the confounder adjusted models (before mutual adjustment for each other) to be our best estimate of the unconfounded association of each with cardiovascular risk factors.
Adiponectin levels were not associated with phobic anxiety in either crude or adjusted models or after mutual adjustment for leptin.
Adjusting for confounders, and mutual adjustment for other parent smoking, attenuated associations in a similar way to that observed for maternal smoking.
Associations observed in the confounder adjusted model (model 3 in tables 1, 2 & 3) were largely unchanged by mutual adjustment for 25(OH D, PTH and adjusted calcium (model 4 in tables 1, 2, & 3).
We also considered potential confounding by other dietary factors, including whole grains and fats, mutual adjustment for meat mutagens (e.g., BaP adjusted for HCAs), as well as energy adjustment, including alcohol intake.
Two sets of multivariable models were estimated, the first were adjusted for these covariates and the second set also included mutual adjustment for each of the other insulin-related biomarkers being assessed here.
All models were adjusted for parental education, parental age and number of children with mutual adjustment for all exposure variables.
With mutual adjustment for each other, these associations remained essentially unchanged.
Table 4 shows the results from two separate models that included mutual adjustment for quintiles of the average annual dose of five NSAID classes.
In a model with mutual adjustment for 5 NSAID classes, propionates (0.89; 0.84–0.95) and arylacetic acids (0.94; 0.88–1.00) were inversely associated with disease risk whereas any use of aspirin was not (OR = 1.01 [95%0.95 1.07]).
As before, CLR models were used to estimates ORs associated with drug use in each period with mutual adjustment for exposure in other periods as well as adjustment for screening predictors.
