Table 3.
CLOCK genotypes | Cases | Person-y | Incidence ratea | Model 1 | Model 2 | ||||
---|---|---|---|---|---|---|---|---|---|
HR | 95 % CI | P value | HR | 95 % CI | P value | ||||
Stroke | |||||||||
Dominant model | |||||||||
CC | 43 | 5780.3 | 7.4 | 1.00 | (Reference) | 1.00 | (Reference) | ||
CG + GG | 43 | 9306.9 | 4.6 | 0.61 | (0.40–0.93) | 0.022 | 0.61 | (0.40–0.94) | 0.024 |
P (interaction CLOCK × T2D status) | 0.016 | 0.018 | |||||||
Myocardial infraction | |||||||||
Dominant model | |||||||||
CC | 24 | 5479.4 | 4.4 | 1.00 | (Reference) | 1.00 | (Reference) | ||
CG + GG | 40 | 9057.8 | 4.4 | 0.99 | (0.60–1.65) | 0.982 | 1.01 | (0.61–1.70) | 0.941 |
P (interaction CLOCK × T2D status) | 0.906 | 0.922 |
Model 1: adjusted for sex, age, center and dietary intervention group
Model 2: adjusted for variables in model 1 plus BMI, drinking, smoking, physical activity, medication (hypertension, dyslipemia and glucose), adherence to the Mediterranean Diet and total energy intake at baseline
P for interaction terms between the CLOCK SNP (as dominant) with T2D in determining stroke or myocardial infarction were estimated in the corresponding multivariable models in the whole population
aCrude incidence rates were expressed per 1000 person-years of follow-up