particular model, calcium supplement use was associated
with a barely significant, slight increase risk of incident CAC
(RR=1.12 [1.00–1.26], P=0.047).
Therefore, we further examined the association of quintiles
of calcium intake with risk of incident CAC stratified by
nonusers and users of calcium supplements, comparing
nonsupplement users in quintile 1 as reference (Table 9).
We found that there was a signal for increased risk of incident
CAC among users of calcium supplements across the first 4
quintiles of calcium intake, with greatest risk noted among
calcium supplement users with the lowest total calcium intake
(quintile 1; RR, 1.41 [1.02–1.97]). For quintile 5, the
previously noted inverse association of high calcium intake
with incident CAC was attenuated among calcium supplement
users (0.91 [0.72–1.15]) versus quintile 5 of intake among
nonsupplement users (0.74 [0.51–1.07]). However, there was
no statistically significant interaction of calcium supplement
use with total calcium intake for quintiles 2 to 5 (P interaction,
>0.05 for all).
Among those with prevalent CAC at the baseline exam,
calcium intake was not associated with an increase in CAC
progression over an average of 10 years of follow-up
(Table 10). This lack of association persisted even when we
considered calcium as a continuous variable and logtransformed
CAC (Dlog CAC=0.0004 [0.047 to 0.046])
per gram of calcium consumed per day.