Participants were 125 youth, aged 8-17 years, with a primary diagnosis of SAD, who were randomly assigned to generic CBT (CBT-GEN), social anxiety specific CBT (CBT-SAD) or a wait list control (WLC).
Some evidence suggests equivalence between tCBT and diagnosis-specific CBT (dxCBT), however more investigations are necessary to clarify any difference in efficacy.
The risk of CBT was nonsignificantly increased in relation to the inefficient PON1 promoter allele [per PON1(-108T) allele, relative to PON1(-108CC): odds ratio (OR) = 1.4; 95% confidence interval (CI), 1.0-2.2; p-value for trend = 0.07].
There was weak evidence of a reduced risk of CBT for the MTRR 66GG genotype in the child or father: ORs 0.71 [95% confidence interval (CI), 0.48-1.07]; 0.54 (95% CI, 0.34-0.87), respectively.
We analyzed population-based case-control data to examine whether CBT is associated with the functional genetic polymorphisms PON1C-108T, PON1Q192R, PON1L55M, BCHEA539T, FMO1C-9536A, FMO3E158K, ALDH3A1S134A, and GSTT1 (null).
We believe that congenital tritanopia and DIJOA are distinct disease entities and that the blue cone ERG is a key factor in the differential diagnosis.