Inflammation and oxidative stress play important roles in colorectal
carcinogenesis. There is strong evidence that
calcium reduces risk for
colorectal neoplasms, possibly through its ability to bind
bile acids and prevent their colonic toxicity (which occurs via an oxidative mechanism and results in an inflammatory response). In a previously reported pilot, randomized, controlled trial among sporadic colorectal
adenoma patients we found that those on 2.0 g/day of
calcium, relative to those on placebo, had an estimated drop in a combined
cytokine z-score of 48% (P = 0.18) over 6 months. To follow-up these promising preliminary findings, we tested the efficacy of two doses of supplemental
calcium (1.0 or 2.0 g/day) relative to placebo on modulating circulating
biomarkers of
inflammation [
C-reactive protein (CRP) and 10
cytokines] and oxidative stress (F2-isoprostanes) over a 4-month treatment period among 193 patients with previous sporadic, colorectal
adenoma in a randomized, double-blinded, placebo-controlled clinical trial. The
inflammation markers were measured in plasma using electrochemiluminescence detection-based immunoassays, and
F2-isoprostanes were measured in plasma using gas chromatography-mass spectrometry. Over a 4-month treatment period, we found no appreciable effects of
calcium on CRP,
cytokines, or
F2-isoprostanes (P > 0.4), overall or within strata of several major risk factors for colorectal
carcinogenesis, such as body mass index and regular use of nonsteroidal anti-inflammatory drugs. Overall, our results provide no evidence that
calcium supplementation favorably modulates concentrations of circulating
biomarkers of
inflammation or oxidative stress over 4 months among patients with a previous colorectal
adenoma.